Updated on 2021/07/09

写真a

 
BANDO, Yasuko K
 
Organization
Nagoya University Hospital Cardiology Lecturer
Graduate School
Graduate School of Medicine
Title
Lecturer

Degree 1

  1. Medical Doctor ( 1996.3   Mie University ) 

Research Interests 1

  1. vasculogenesis angiogenesis heart failure diabetes

Research Areas 2

  1. Others / Others  / Circulatory Organs Internal Medicine

  2. Life Science / Cardiology

Current Research Project and SDGs 2

  1. Molecular mechanism of cardiac redemoing in heart failure

  2. Oncocardiology

Research History 3

  1. Nagoya University   Innovative Research Center for Preventive Medical Engineering   Associate Professor

    2013.12

  2. Nagoya University   University Lecturer

    2009.3 - 2011.3

  3. 2006-2007 Visiting researcher, Department of Cardiology, Nagoya University Graduate School of Medicine2007- Assistant professor, Department of Cardiology, Nagoya University Graduate School of Medici

    2006.4

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    Country:Japan

Education 2

  1. Mie University   Graduate School, Division of Medical Sciences   Internal Medicine

    1994.4 - 1998.3

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    Country: Japan

  2. Mie University   Faculty of Medicine

    1986.4 - 1992.3

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    Country: Japan

Professional Memberships 16

  1. ISHR Japan section

    2019.4

  2. JOCS

    2018.12

  3. The Japanese Circulation Society   FJCS

  4. Japanese Heart Failure Society

  5. Japan Society of Circulation Research

  6. The Japan Atherosclerosis Society

  7. American Heart Association

  8. ヨーロッパ心臓病学会

  9. 日本炎症・再生医学会

  10. 日本心臓病学会

  11. J-ISCP

  12. 心筋生検研究会   幹事

  13. 日本内科学会   東海支部評議員

  14. American Diabetes Society

  15. Japanese Diabetes Society

  16. JDS

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Committee Memberships 3

  1. Department of Cardiology, Nagoya University   Head of Cardiology Office  

    2020.10   

  2. 愛知県医師会男女共同参画委員   委員  

    2018.4   

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    Committee type:Other

  3. 日本循環器学会ダイバーシティ委員会   委員  

    2015.4   

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    Committee type:Academic society

Awards 2

  1. Best Reviewer Award

    2017.3   Japanese Circulation Society  

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    Award type:Honored in official journal of a scientific society, scientific journal  Country:Japan

  2. CPIS award,

    2001.3   65th Annual Scientific Meeting of the Japanese Circulation Society .  

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    Country:Japan

 

Papers 71

  1. . Dipeptidyl Peptidase-4 Modulates Left Ventricular Dysfunction in Chronic Heart Failure via Angiogenesis-Dependent and-Independent Actions. Reviewed

    Shigeta T, Aoyama M, Bando YK, Monji A, Mitsui T, Takatsu M, Cheng XW, Okumura T, Hirashiki A, Nagata K, Murohara T

    Circulation   Vol. 126 ( 15 ) page: 1838   2012.10

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  2. Cancer and Coronary Heart Disease - To Bleed or Not to Bleed, That Is the Question -

    Bando Yasuko K.

    CIRCULATION JOURNAL   Vol. 85 ( 6 ) page: 847 - 849   2021.6

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    Language:Japanese   Publisher:一般社団法人 日本循環器学会  

    DOI: 10.1253/circj.CJ-21-0174

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  3. Important Role of Concomitant Lymphangiogenesis for Reparative Angiogenesis in Hindlimb Ischemia

    Pu Zhongyue, Shimizu Yuuki, Tsuzuki Kazuhito, Suzuki Junya, Hayashida Ryo, Kondo Kazuhisa, Fujikawa Yusuke, Unno Kazumasa, Ohashi Koji, Takefuji Mikito, Bando Yasuko K., Ouchi Noriyuki, Calvert John W., Shibata Rei, Murohara Toyoaki

    ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY   Vol. 41 ( 6 ) page: 2006 - 2018   2021.6

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    Language:Japanese   Publisher:Arteriosclerosis, Thrombosis, and Vascular Biology  

    OBJECTIVE: Lymphatic vessels are distributed throughout the body and tightly collaborate with blood vessels to maintain tissue homeostasis. However, the functional roles of lymphangiogenesis in the process of reparative angiogenesis in ischemic tissues are largely unknown. Accordingly, we investigated potential roles of lymphangiogenesis using a mouse model of ischemia-induced angiogenesis. APPROACH AND RESULTS: Male C57BL/6J mice were subjected to unilateral hindlimb ischemia, in which not only angiogenesis but also lymphangiogenesis was induced. Next, the excessive and prolonged tissue edema model significantly deteriorated reparative angiogenesis and blood perfusion recovery in ischemic limbs. Finally, implantation of adipose-derived regenerative cells augmented ischemia-induced lymphangiogenesis, which was accompanied by reduced tissue edema and inflammation, resulting in improving reparative angiogenesis and blood perfusion recovery. In addition, inhibition of lymphangiogenesis by MAZ51, a specific VEGFR3 (vascular endothelial cell growth factor receptor 3) inhibitor, resulted in enhanced inflammatory cell infiltration, gene expression of TNF (tumor necrosis factor)-α, IL (interleukin)-1β, IL-6, TGF (transforming growth factor)β, angiostatin, vasohibin, and endostatin, and tissue edema, resulting in reduced angiogenesis. CONCLUSIONS: The lymphatic system may have a clearance role of tissue edema and inflammation, which contribute to functional reparative angiogenesis in response to tissue ischemia. Modulation of lymphangiogenesis would become a novel therapeutic strategy for severe ischemic disease in addition to ordinary vascular intervention and therapeutic angiogenesis.

    DOI: 10.1161/ATVBAHA.121.316191

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  4. Omentin attenuates angiotensin II-induced abdominal aortic aneurysm formation in apolipoprotein-E knockout mice.

    Fang L, Ohashi K, Otaka N, Ogawa H, Hiramatsu-Ito M, Kawanishi H, Bando YK, Shibata R, Shimizu Y, Kato K, Takikawa T, Ozaki Y, Takefuji M, Murohara T, Ouchi N

    Cardiovascular research     2021.5

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    DOI: 10.1093/cvr/cvab179

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  5. Ⅱ. Clinical Management of Heart Failure in Cancer Patients

    Bando Y.K.

    Gan to kagaku ryoho. Cancer & chemotherapy   Vol. 48 ( 5 ) page: 655 - 659   2021.5

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  6. [Ⅱ. Clinical Management of Heart Failure in Cancer Patients].

    Bando YK

    Gan to kagaku ryoho. Cancer & chemotherapy   Vol. 48 ( 5 ) page: 655 - 659   2021.5

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  7. The aging-induced hyperexcretion of glucose-dependent insulinotropic peptide is essential for the healthy cardiac remodeling by prevention of cardiac ceramide accumulation

    Bando Y. Kureishi, Remina Y. R., Kamihara T. K., Nishimura K. N., Murohara T. M.

    EUROPEAN HEART JOURNAL   Vol. 41   page: 3615 - 3615   2020.11

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  8. Cardiac aging is regulated by autophagic disorder mediated by chronic inflammation via the Rubicon/NOX4 pathway

    Kamihara T., Bando Y. K., Murohara T.

    EUROPEAN HEART JOURNAL   Vol. 41   page: 842 - 842   2020.11

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  9. Heart Failure and Cancer - A Comorbid Risk That Is No Longer Underestimated -

    Kazama Shingo, Bando Yasuko K., Murohara Toyoaki

    CIRCULATION JOURNAL   Vol. 84 ( 10 ) page: 1689 - 1690   2020.10

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    Language:Japanese   Publisher:一般社団法人 日本循環器学会  

    DOI: 10.1253/circj.CJ-20-0888

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  10. Myocardial Vasculitis Associated With the Immune Checkpoint Inhibitor Pembrolizumab

    Oishi H., Morimoto R., Shimoyama Y., Kuroda K., Urata T., Kondo T., Okumura T., Bando Y.K., Akiyama M., Murohara T.

    JACC: Case Reports   Vol. 2 ( 12 ) page: 1937 - 1941   2020.10

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    Recent developments in immune checkpoint inhibitors (ICIs) have provided new treatment strategies for advanced cancer. However, ICIs lead to an imbalance between T cell–mediated inflammatory responses and immune tolerance in the myocardium. Here we report the first case that implicates the contribution of ICI-induced vasculitis to myocardial injury. (Level of Difficulty: Intermediate.)

    DOI: 10.1016/j.jaccas.2020.07.028

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  11. Protein Kinase N Promotes Stress-Induced Cardiac Dysfunction Through Phosphorylation of Myocardin-Related Transcription Factor A and Disruption of Its Interaction With Actin

    Sakaguchi Teruhiro, Takefuji Mikito, Wettschureck Nina, Hamaguchi Tomonari, Amano Mutsuki, Kato Katsuhiro, Tsuda Takuma, Eguchi Shunsuke, Ishihama Sohta, Mori Yu, Yura Yoshimitsu, Yoshida Tatsuya, Unno Kazumasa, Okumura Takahiro, Ishii Hideki, Shimizu Yuuki, Bando Yasuko K., Ohashi Koji, Ouchi Noriyuki, Enomoto Atsushi, Offermanns Stefan, Kaibuchi Kozo, Murohara Toyoaki

    CIRCULATION   Vol. 140 ( 21 ) page: 1737 - 1752   2019.11

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    Language:Japanese   Publisher:Circulation  

    Background: Heart failure is a complex syndrome that results from structural or functional impairment of ventricular filling or blood ejection. Protein phosphorylation is a major and essential intracellular mechanism that mediates various cellular processes in cardiomyocytes in response to extracellular and intracellular signals. The RHOA-associated protein kinase (ROCK/Rho-kinase), an effector regulated by the small GTPase RHOA, causes pathological phosphorylation of proteins, resulting in cardiovascular diseases. RHOA also activates protein kinase N (PKN); however, the role of PKN in cardiovascular diseases remains unclear. Methods: To explore the role of PKNs in heart failure, we generated tamoxifen-inducible, cardiomyocyte-specific PKN1- and PKN2-knockout mice by intercrossing the αMHC-CreERT2 line with Pkn1flox/flox and Pkn2flox/flox mice and applied a mouse model of transverse aortic constriction- and angiotensin II-induced heart failure. To identify a novel substrate of PKNs, we incubated GST-tagged myocardin-related transcription factor A (MRTFA) with recombinant GST-PKN-catalytic domain or GST-ROCK-catalytic domain in the presence of radiolabeled ATP and detected radioactive GST-MRTFA as phosphorylated MRTFA. Results: We demonstrated that RHOA activates 2 members of the PKN family of proteins, PKN1 and PKN2, in cardiomyocytes of mice with cardiac dysfunction. Cardiomyocyte-specific deletion of the genes encoding Pkn1 and Pkn2 (cmc-PKN1/2 DKO) did not affect basal heart function but protected mice from pressure overload- and angiotensin II-induced cardiac dysfunction. Furthermore, we identified MRTFA as a novel substrate of PKN1 and PKN2 and found that MRTFA phosphorylation by PKN was considerably more effective than that by ROCK in vitro. We confirmed that endogenous MRTFA phosphorylation in the heart was induced by pressure overload- and angiotensin II-induced cardiac dysfunction in wild-type mice, whereas cmc-PKN1/2 DKO mice suppressed transverse aortic constriction- and angiotensin II-induced phosphorylation of MRTFA. Although RHOA-mediated actin polymerization accelerated MRTFA-induced gene transcription, PKN1 and PKN2 inhibited the interaction of MRTFA with globular actin by phosphorylating MRTFA, causing increased serum response factor-mediated expression of cardiac hypertrophy- and fibrosis-associated genes. Conclusions: Our results indicate that PKN1 and PKN2 activation causes cardiac dysfunction and is involved in the transition to heart failure, thus providing unique targets for therapeutic intervention for heart failure.

    DOI: 10.1161/CIRCULATIONAHA.119.041019

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  12. Impaired autophagic off-rate causes cardiac aging in progeria mouse model

    Kamihara T., Bando Y. Kureishi, Nishimura K., Yasheng R., Ozaki R., Murohara T.

    EUROPEAN HEART JOURNAL   Vol. 40   page: 1321 - 1321   2019.10

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  13. Glucose-dependent insulinotropic peptide is essential for maintenance of cardiac lipid metabolism via FGF21-dependent pathway

    Remina Y., Bando Y. Kureishi, Ozaki R., Kamihara T., Nishimura K., Murohara T.

    EUROPEAN HEART JOURNAL   Vol. 40   page: 2094 - 2094   2019.10

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  14. Roles of the Mesenchymal Stromal/Stem Cell Marker Meflin in Cardiac Tissue Repair and the Development of Diastolic Dysfunction

    Hara Akitoshi, Kobayashi Hiroki, Asai Naoya, Saito Shigeyoshi, Higuchi Takahiro, Kato Katsuhiro, Okumura Takahiro, Bando Yasuko K., Takefuji Mikito, Mizutani Yasuyuki, Miyai Yuki, Saito Shoji, Maruyama Shoichi, Maeda Keiko, Ouchi Noriyuki, Nagasaka Arata, Miyata Takaki, Mii Shinji, Kioka Noriyuki, Worthley Daniel L., Murohara Toyoaki, Takahashi Masahide, Enomoto Atsushi

    CIRCULATION RESEARCH   Vol. 125 ( 4 ) page: 414 - 430   2019.8

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    Rationale: Myofibroblasts have roles in tissue repair following damage associated with ischemia, aging, and inflammation and also promote fibrosis and tissue stiffening, causing organ dysfunction. One source of myofibroblasts is mesenchymal stromal/stem cells that exist as resident fibroblasts in multiple tissues. We previously identified meflin (mesenchymal stromal cell-and fibroblast-expressing Linx paralogue), a glycosylphosphatidylinositol-Anchored membrane protein, as a specific marker of mesenchymal stromal/stem cells and a regulator of their undifferentiated state. The roles of meflin in the development of heart disease, however, have not been investigated. Objective: We examined the expression of meflin in the heart and its involvement in cardiac repair after ischemia, fibrosis, and the development of heart failure. Methods and Results: We found that meflin has an inhibitory role in myofibroblast differentiation of cultured mesenchymal stromal/stem cells. Meflin expression was downregulated by stimulation with TGF (transforming growth factor)-β, substrate stiffness, hypoxia, and aging. Histological analysis revealed that meflin-positive fibroblastic cells and their lineage cells proliferated in the hearts after acute myocardial infarction and pressure-overload heart failure mouse models. Analysis of meflin knockout mice revealed that meflin is essential for the increase in the number of cells that highly express type I collagen in the heart walls after myocardial infarction induction. When subjected to pressure overload by transverse aortic constriction, meflin knockout mice developed marked cardiac interstitial fibrosis with defective compensation mechanisms. Analysis with atomic force microscopy and hemodynamic catheterization revealed that meflin knockout mice developed stiff failing hearts with diastolic dysfunction. Mechanistically, we found that meflin interacts with bone morphogenetic protein 7, an antifibrotic cytokine that counteracts the action of TGF-β and augments its intracellular signaling. Conclusions: These data suggested that meflin is involved in cardiac tissue repair after injury and has an inhibitory role in myofibroblast differentiation of cardiac fibroblastic cells and the development of cardiac fibrosis.

    DOI: 10.1161/CIRCRESAHA.119.314806

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  15. Impaired Autophagic Off-rate Causes Cardiac Aging in Progeria Mouse Model

    Bando Yasuko K., Kamihara Takahiro, Murohara Toyoaki

    CIRCULATION RESEARCH   Vol. 125   2019.8

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  16. Cardiomyocytes capture stem cell-derived, anti-apoptotic microRNA-214 via clathrin-mediated endocytosis in acute myocardial infarction

    Eguchi Shunsuke, Takefuji Mikito, Sakaguchi Teruhiro, Ishihama Sohta, Mori Yu, Tsuda Takuma, Takikawa Tomonobu, Yoshida Tatsuya, Ohashi Koji, Shimizu Yuuki, Hayashida Ryo, Kondo Kazuhisa, Bando Yasuko K., Ouchi Noriyuki, Murohara Toyoaki

    JOURNAL OF BIOLOGICAL CHEMISTRY   Vol. 294 ( 31 ) page: 11665 - 11674   2019.8

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    Extracellular vesicles (EVs) have emerged as key mediators of intercellular communication that have the potential to improve cardiac function when used in cell-based therapy. However, the means by which cardiomyocytes respond to EVs remains unclear. Here, we sought to clarify the role of exosomes in improving cardiac function by investigating the effect of cardiomyocyte endocytosis of exosomes from mesenchymal stem cells on acute myocardial infarction (MI). Exposing cardiomyocytes to the culture supernatant of adipose-derived regenerative cells (ADRCs) prevented cardiomyocyte cell damage under hypoxia in vitro. In vivo, the injection of ADRCs into the heart simultaneous with coronary artery ligation decreased overall cardiac infarct area and prevented cardiac rupture after acute MI. Quantitative RT-PCR– based analysis of the expression of 35 known anti-apoptotic and secreted microRNAs (miRNAs) in ADRCs revealed that ADRCs express several of these miRNAs, among which miR-214 was the most abundant. Of note, miR-214 silencing in ADRCs significantly impaired the anti-apoptotic effects of the ADRC treatment on cardiomyocytes in vitro and in vivo. To examine cardiomyocyte endocytosis of exosomes, we cultured the cardiomyocytes with ADRC-derived exosomes labeled with the fluorescent dye PKH67 and found that hypoxic culture conditions increased the levels of the labeled exosomes in cardiomyocytes. Chlorpromazine, an inhibitor of clathrin-mediated endocytosis, significantly suppressed the ADRC-induced decrease of hypoxia-damaged cardiomyocytes and also decreased hypoxia-induced cardiomyocyte capture of both labeled EVs and extracellular miR-214 secreted from ADRCs. Our results indicate that clathrin-mediated endocytosis in cardiomyocytes plays a critical role in their uptake of circulating, exosome-associated miRNAs that inhibit apoptosis.

    DOI: 10.1074/jbc.RA119.007537

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  17. Left ventricular phase entropy: Novel prognostic predictor in patients with dilated cardiomyopathy and narrow QRS

    Kano Naoaki, Okumura Takahiro, Isobe Satoshi, Sawamura Akinori, Watanabe Naoki, Fukaya Kenji, Mori Hiroaki, Morimoto Ryota, Kato Katsuhiko, Bando Yasuko K., Murohara Toyoaki

    JOURNAL OF NUCLEAR CARDIOLOGY   Vol. 25 ( 5 ) page: 1677 - 1687   2018.10

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    DOI: 10.1007/s12350-017-0807-1

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  18. The Selvester QRS score as a predictor of cardiac events in nonischemic dilated cardiomyopathy

    Hiraiwa Hiroaki, Okumura Takahiro, Sawamura Akinori, Sugiura Yuki, Kondo Toru, Watanabe Naoki, Aoki Soichiro, Ichii Takeo, Kitagawa Katsuhide, Kano Naoaki, Fukaya Kenji, Furusawa Kenji, Morimoto Ryota, Takeshita Kyosuke, Bando Yasuko K., Murohara Toyoaki

    JOURNAL OF CARDIOLOGY   Vol. 71 ( 3-4 ) page: 284 - 290   2018

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    DOI: 10.1016/j.jjcc.2017.09.002

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  19. The Selvester QRS score as a predictor of cardiac events in nonischemic dilated cardiomyopathy (vol 71, pg 284, 2018)

    Hiraiwa Hiroaki, Okumura Takahiro, Sawamura Akinori, Sugiura Yuki, Kondo Toru, Watanabe Naoki, Aoki Soichiro, Ichii Takeo, Kitagawa Katsuhide, Kano Naoaki, Fukaya Kenji, Furusawa Kenji, Morimoto Ryota, Takeshita Kyosuke, Bando Yasuko K., Murohara Toyoaki

    JOURNAL OF CARDIOLOGY   Vol. 72 ( 1-2 ) page: 178 - 178   2018

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    DOI: 10.1016/j.jjcc.2018.02.001

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  20. Development and Validation of a Novel Cuff-Less Blood Pressure Monitoring Device.

    Watanabe N, Bando YK, Kawachi T, Yamakita H, Futatsuyama K, Honda Y, Yasui H, Nishimura K, Kamihara T, Okumura T, Ishii H, Kondo T, Murohara T

    JACC. Basic to translational science   Vol. 2 ( 6 ) page: 631 - 642   2017.12

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    Ordinary cuff-based blood pressure–monitoring devices remain a technical limitation that disturbs activities of daily life. Here we report a novel system for the cuff-less blood pressure estimation (CLB) that requires only 1 sensor for photoplethysmography. The present study is the first report to validate and assess the clinical application of the CLB in accordance with the latest wearable device standard (issued by the Institute of Electrical and Electronics Engineers, standard 1708-2014). Our CLB is expected to offer a flexible and wearable device that permits blood pressure monitoring in more continuous and stress-free settings.

    DOI: 10.1016/j.jacbts.2017.07.015

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  21. Sokolow-Lyon voltage is suitable for monitoring improvement in cardiac function and prognosis of patients with idiopathic dilated cardiomyopathy

    Fukaya Kenji, Takeshita Kyosuke, Okumura Takahiro, Hiraiwa Hiroaki, Aoki Soichiro, Ichii Takeo, Sugiura Yuki, Kitagawa Katsuhide, Kondo Toru, Watanabe Naoki, Kano Naoaki, Furusawa Kenji, Sawamura Akinori, Morimoto Ryota, Bando Yasuko, Murohara Toyoaki

    ANNALS OF NONINVASIVE ELECTROCARDIOLOGY   Vol. 22 ( 5 )   2017.9

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    DOI: 10.1111/anec.12431

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  22. Dipeptidyl Peptidase-4 Regulates Hematopoietic Stem Cell Activation in Response to Chronic Stress

    Zhu Enbo, Hu Lina, Wu Hongxian, Piao Limei, Zhao Guangxian, Inoue Aiko, Kim Weon, Yu Chenglin, Xu Wenhu, Bando Yasuko K., Li Xiang, Lei Yanna, Hao Chang-Ning, Takeshita Kyosuke, Kim Woo-Shik, Okumura Kenji, Murohara Toyoaki, Kuzuya Masafumi, Cheng Xian Wu

    JOURNAL OF THE AMERICAN HEART ASSOCIATION   Vol. 6 ( 7 )   2017.7

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    Background-DPP4 (Dipeptidyl peptidase-4)-GLP-1 (glucagon-like peptide-1) and its receptor (GLP-1R) axis has been involved in several intracellular signaling pathways. The Adrβ3 (β3-adrenergic receptor)/CXCL12 (C-X-C motif chemokine 12) signal was required for the hematopoiesis. We investigated the novel molecular requirements between DPP4-GLP-1/ GLP-1 and Adrβ3/CXCL12 signals in bone marrow (BM) hematopoietic stem cell (HSC) activation in response to chronic stress. Methods and Results-Male 8-week-old mice were subjected to 4-week intermittent restrain stress and orally treated with vehicle or the DPP4 inhibitor anagliptin (30 mg/kg per day). Control mice were left undisturbed. The stress increased the blood and brain DPP4 levels, the plasma epinephrine and norepinephrine levels, and the BM niche cell Adrβ3 expression, and it decreased the plasma GLP-1 levels and the brain GLP-1R and BM CXCL12 expressions. These changes were reversed by DPP4 inhibition. The stress activated BM sca-1highc-KithighCD48lowCD150high HSC proliferation, giving rise to high levels of blood leukocytes and monocytes. The stress-activated HSC proliferation was reversed by DPP4 depletion and by GLP-1R activation. Finally, the selective pharmacological blocking of Adrβ3 mitigated HSC activation, accompanied by an improvement of CXCL12 gene expression in BM niche cells in response to chronic stress. Conclusions-These findings suggest that DPP4 can regulate chronic stress-induced BM HSC activation and inflammatory cell production via an Adrβ3/CXCL12-dependent mechanism that is mediated by the GLP-1/GLP-1R axis, suggesting that the DPP4 inhibition or the GLP-1R stimulation may have applications for treating inflammatory diseases.

    DOI: 10.1161/JAHA.117.006394

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  23. Effect of sitagliptin on the echocardiographic parameters of left ventricular diastolic function in patients with type 2 diabetes: a subgroup analysis of the PROLOGUE study

    Yamada Hirotsugu, Tanaka Atsushi, Kusunose Kenya, Amano Rie, Matsuhisa Munehide, Daida Hiroyuki, Ito Masaaki, Tsutsui Hiroyuki, Nanasato Mamoru, Kamiya Haruo, Bando Yasuko K., Odawara Masato, Yoshida Hisako, Murohara Toyoaki, Sata Masataka, Node Koichi

    CARDIOVASCULAR DIABETOLOGY   Vol. 16 ( 1 ) page: 63   2017.5

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    Background: Diabetes is associated closely with an increased risk of cardiovascular events, including diastolic dysfunction and heart failure that leads to a shortening of life expectancy. It is therefore extremely valuable to evaluate the impact of antidiabetic agents on cardiac function. However, the influence of dipeptidyl peptidase 4 inhibitors on cardiac function is controversial and a major matter of clinical concern. We therefore evaluated the effect of sitagliptin on echocardiographic parameters of diastolic function in patients with type 2 diabetes as a sub-analysis of the PROLOGUE study. Methods: Patients in the PROLOGUE study were assigned randomly to either add-on sitagliptin treatment or conventional antidiabetic treatment. Of the 463 patients in the overall study, 115 patients (55 in the sitagliptin group and 60 in the conventional group) who had complete echocardiographic data of the ratio of peak early diastolic transmitral flow velocity (E) to peak early diastolic mitral annular velocity (e') at baseline and after 12 and 24 months were included in this study. The primary endpoint of this post hoc sub-analysis was a comparison of the changes in the ratio of E to e' (E/e') between the two groups from baseline to 24 months. Results: The baseline-adjusted change in E/e' during 24 months was significantly lower in the sitagliptin group than in the conventional group (-0.18 ± 0.55 vs. 1.91 ± 0.53, p = 0.008), irrespective of a higher E/e' value at baseline in the sitagliptin group. In analysis of covariance, sitagliptin treatment was significantly associated with change in E/e' over 24 months (β = -9.959, p = 0.001), independent of other clinical variables at baseline such as blood pressure, HbA1c, and medications for diabetes. Changes in other clinical variables including blood pressure and glycemic parameters, and echocardiographic parameters, such as cardiac structure and systolic function, were comparable between the two groups. There was also no significant difference in the serum levels of N-terminal-pro brain natriuretic peptide and high-sensitive C-reactive protein between the two groups during the study period. Conclusions: Adding sitagliptin to conventional antidiabetic regimens in patients with T2DM for 24 months attenuated the annual exacerbation in the echocardiographic parameter of diastolic dysfunction (E/e') independent of other clinical variables such as blood pressure and glycemic control. Trial registration UMIN000004490 (University Hospital Medical Information Network Clinical Trials). https://upload.umin.ac.jp/cgi-open-bin/ctr_e/ctr_view.cgi?recptno=R000005356 ; registered November 1, 2010

    DOI: 10.1186/s12933-017-0546-2

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  24. Long-Term Pathological Follow-Up of Myocardium in a Carrier of Duchenne Muscular Dystrophy With Dilated Cardiomyopathy

    Kondo Toru, Okumura Takahiro, Takefuji Mikito, Hiraiwa Hiroaki, Sugiura Yuki, Watanabe Naoki, Aoki Soichiro, Ichii Takeo, Kitagawa Katsuhide, Kano Naoaki, Fukaya Kenji, Furusawa Kenji, Sawamura Akinori, Morimoto Ryota, Bando Yasuko K., Takemura Genzou, Murohara Toyoaki

    CIRCULATION-HEART FAILURE   Vol. 10 ( 3 ) page: e003826   2017.3

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    DOI: 10.1161/CIRCHEARTFAILURE.117.003826

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  25. Biphasic Force-Frequency Relation Predicts Primary Cardiac Events in Patients With Hypertrophic Cardiomyopathy

    Morimoto Ryota, Okumura Takahiro, Bando Yasuko K., Fukaya Kenji, Sawamura Akinori, Kawase Haruya, Shimizu Shinya, Shimazu Shuzo, Hirashiki Akihiro, Takeshita Kyosuke, Murohara Toyoaki

    CIRCULATION JOURNAL   Vol. 81 ( 3 ) page: 368 - 375   2017.3

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    <p><b><i>Background:</i></b>The force-frequency relation (FFR) is a hemodynamic index of the chronotropic relationship between left ventricular (LV) systolic function (percent change in dP/dt<sub>max</sub>) and elevation of heart rate. FFR is a marker of myocardial contractile reserve and follows an upward slope in healthy myocardium [monophasic FFR (MoF)], a pattern that becomes biphasic (BiF) under pathological conditions. However, it remains uncertain whether the FFR determines a patient's prognosis. We investigated the promising role of the FFR as a predictor of cardiac events in the setting of hypertrophic cardiomyopathy (HCM).</p><p><b><i>Methods and Results:</i></b>A total of 113 consecutive patients with HCM (New York Heart Association (NYHA) class I–II) were retrospectively evaluated; 27 (23.9%) had a BiF pattern and they experienced a higher incidence of cardiac events compared with those showing an MoF pattern (median follow-up, 4.7 years; P<0.001). Furthermore, Cox proportional hazard regression analysis revealed that the LV end-diastolic volume index (hazard ratio: 1.051, P=0.014) and BiF pattern (hazard ratio: 15.260, P=0.001) were independent predictors of primary cardiac events. Interestingly, abnormal reductions in myocardial regulatory molecules related to contractility (SERCA2α) were observed exclusively in the patients exhibiting a BiF pattern.</p><p><b><i>Conclusions:</i></b>The FFR reflects latent myocardial abnormalities and predicts cardiac events in the setting of HCM, even during the asymptomatic stages of the disease.</p>

    DOI: 10.1253/circj.CJ-16-1007

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  26. Asian Perspective of the EMPA-REG OUTCOME Study

    Bando Yasuko K., Murohara Toyoaki

    CIRCULATION JOURNAL   Vol. 81 ( 2 ) page: 155 - 157   2017.2

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    DOI: 10.1253/circj.CJ-16-1304

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  27. Myocardial contractile reserve predicts left ventricular reverse remodeling and cardiac events in dilated cardiomyopathy

    Morimoto Ryota, Okumura Takahiro, Hirashiki Akihiro, Ishii Hideki, Ichii Takeo, Aoki Soichiro, Furusawa Kenji, Hiraiwa Hiroaki, Kondo Toru, Watanabe Naoki, Kano Naoaki, Fukaya Kenji, Sawamura Akinori, Takeshita Kyosuke, Bando Yasuko K., Murohara Toyoaki

    JOURNAL OF CARDIOLOGY   Vol. 70 ( 3-4 ) page: 303 - 309   2017

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    DOI: 10.1016/j.jjcc.2017.02.005

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  28. Cholesterol metabolism as a prognostic marker in patients with mildly symptomatic nonischemic dilated cardiomyopathy

    Sawamura Akinori, Okumura Takahiro, Hiraiwa Hiroaki, Aoki Soichiro, Kondo Toru, Ichii Takeo, Furusawa Kenji, Watanabe Naoki, Kano Naoaki, Fukaya Kenji, Morimoto Ryota, Bando Yasuko K., Murohara Toyoaki

    JOURNAL OF CARDIOLOGY   Vol. 69 ( 5-6 ) page: 888 - 894   2017

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    Background Little is known about whether the alteration of cholesterol metabolism reflects abdominal organ impairments due to heart failure. Therefore, we investigated the prognostic value of cholesterol metabolism by evaluating serum campesterol and lathosterol levels in patients with early-stage nonischemic dilated cardiomyopathy (NIDCM). Methods We enrolled 64 patients with NIDCM (median age 57.5 years, 31% female) with New York Heart Association functional class I/II. Serum campesterol and lathosterol levels were measured in all patients. The patients were then divided into four subsets based on the median non-cholesterol sterol levels (campesterol 3.6 μg/mL, lathosterol 1.4 μg/mL): reference (R-subset), high-campesterol/high-lathosterol; absorption-reduced (A-subset), low-campesterol/high-lathosterol; synthesis-reduced (S-subset), high-campesterol/low-lathosterol; double-reduced (D-subset), low-campesterol/low-lathosterol. Endpoint was a composite of cardiac events, including cardiac-related death, hospitalization for worsening heart failure, and lethal arrhythmia. Results Median brain natriuretic peptide (BNP) level was 114 pg/mL. Mean left ventricular ejection fraction was 31.4%. D-subset had the lowest total cholesterol level and cardiac index and the highest BNP level and pulmonary capillary wedge pressure. D-subset also had the highest cardiac event rate during the mean 3.8 years of follow-up (log-rank p = 0.001). Multivariate regression analysis showed that D-subset was an independent determinant of cardiac events. The receiver operating characteristic curve analysis revealed that total cholesterol <153 mg/dL was a best cut-off value for discrimination of the D-subset. Conclusions The combined reduction of campesterol and lathosterol that indicated intestinal cholesterol absorption and liver synthesis predicts future cardiac events in patients with mildly symptomatic NIDCM.

    DOI: 10.1016/j.jjcc.2016.08.012

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  29. Effect of Standard vs Intensive Blood Pressure Control on the Risk of Recurrent Stroke A Randomized Clinical Trial and Meta-analysis

    Kitagawa Kazuo, Yamamoto Yasumasa, Arima Hisatomi, Maeda Toshiki, Sunami Norio, Kanzawa Takao, Eguchi Kazuo, Kamiyama Kenji, Minematsu Kazuo, Ueda Shinichiro, Rakugi Hiromi, Ohya Yusuke, Kohro Takahide, Yonemoto Koji, Okada Yasushi, Higaki Jitsuo, Tanahashi Norio, Kimura Genjiro, Umemura Satoshi, Matsumoto Masayasu, Shimamoto Kazuaki, Ito Sadayoshi, Saruta Takao, Shimada Kazuyuki, Kario Kazuomi, Saito Yoshihiko, Terayama Yasuo, Toyoda Kazunori, Okura Takafumi, Hoshino Haruhiko, Makino Hirofumi, Uchida Haruhito, Uchiyama Shinichiro, Etani Hideki, Kohriyama Tatsuo, Tomimoto Hidekazu, Yoshio Taku, Kobayashi Shotai, Usami Hiroko, Iihoshi Satoshi, Mikami Takeshi, Mikuni Nobuhiro, Miyata Kei, Murakami Tomohiro, Endo Hideki, Fukui Takahito, Fumoto Kentaro, Hara Keiji, Honjo Kaori, Kinoshita Yusuke, Maeda Masana, Mikamoto Masaaki, Mori Daisuke, Murahashi Takeo, Nomura Ryota, Noro Shusaku, Ogino Tatsuya, Okuma Masahiro, Otake Yasuhumi, Shindo Koichiro, Sugio Hironori, Takada Hidekazu, Takahira Kazuki, Takeuchi Akiko, Watanabe Toshiichi, Yamaguchi Yohei, Abumiya Takeo, Houkin Kiyohiro, Matsumura Shigeki, Murakami Tomohiro, Shinohe Rikiya, Kuroshima Kiyomi, Takizawa Katsumi, Yoshida Kazuto, Morimoto Hideo, Hasebe Naoyuki, Koyama Satoshi, Maruyama Junichi, Irie Shinsuke, Nakano Takahiro, Ogasawara Yukari, Ohkuma Hiroki, Shibanai Kazuo, Hikichi Kentaro, Kobayashi Shinya, Moroi Junta, Nakase Taizen, Okada Takeshi, Takano Daiki, Takenaka Shunsuke, Yoshioka Shotaro, Yanagisawa Toshiharu, Hirata Yutaka, Konno Shu, Sato Tomohiko, Ito Miiko, Kondo Rei, Mori Wataru, Saito Shinjiro, Kokubo Yasuaki, Kato Hideaki, Oyama Hideki, Matsuo Kaneyuki, Matsumoto Masahiro, Nakamura Mari, Koizumi Takayuki, Sato Hiroyuki, Shibata Yasushi, Eguchi Kazuo, Kario Kazuomi, Hashimoto Masaaki, Eguchi Kazuo, Kurita Hideharu, Matsumoto Eiji, Ishiguro Koji, Asakura Ken, Fujimaki Hiroya, Wakabayashi Kazuki, Akaji Kazunori, Horikoshi Tomo, Kano Tadashige, Kanzawa Takao, Katano Takehiro, Kimura Hiroaki, Mihara Ban, Suzuki Kentaro, Takayama Yohei, Ishii Akira, Momomura Sin-ichi, Sugawara Hitoshi, Yamashita Takeshi, Kaneko Uichi, Takahashi Toshie, Arai Toshinari, Tanaka Yoshihiro, Inokuma Shigehisa, Kato Yuji, Tanahashi Norio, Ishige Naoki, Muramatsu Kazuhiro, Nogawa Shigeru, Yoshizaki Takahito, Ohashi Takashi, Suda Sumio, Iguchi Yasuyuki, Mitsumura Hidetaka, Adachi Tomohide, Hoshino Haruhiko, Konoeda Fumie, Oki Koichi, Tanaka Ryota, Urabe Takao, Yamashiro Kazuo, Ito Akihiro, Nakatomi Hirofumi, Shojima Masaaki, Otsuka Kuniaki, Shibata Koichi, Abe Takato, Itoh Yoshiaki, Oki Koichi, Suzuki Norihiro, Kitagawa Kazuo, Toi Sono, Teramoto Tamio, Fukunaga Atsushi, Kujuro Yuki, Ohta Kouichi, Osada Takashi, Shimizu Katuyoshi, Kitagawa Yasuhisa, Tokuoka Kentaro, Omura Masao, Kikyo Hideyuki, Kamide Tomoya, Kitamura Yoshihisa, Miyashita Katsuyoshi, Mori Kentaro, Shima Hiroshi, Tamase Akira, Akutsu Tsugio, Nishiyama Kazutoshi, Takizawa Shunya, Uesugi Tsuyoshi, Ikeda Uichi, Koshikawa Megumi, Yamasaki Saeko, Inoue Atsushi, Matsumoto Yasuko, Yamaguchi Kazuyoshi, Hirose Genjirou, Kontani Satoshi, Takasawa Kazuya, Hirahara Katsumi, Kodama Makoto, Yagihara Nobue, Hata Takashi, Hori Makoto, Oda Rokuhei, Kubo Ayuka, Okuda Satoshi, Yamada Kentaro, Takeuchi Hiroki, Araki Yoshio, Ito Mizuki, Senda Joe, Wakabayashi Toshihiko, Ito Shinji, Mutoh Tatsuro, Kawase Yukinori, Ando Fumio, Okamoto Shinya, Shimada Takuya, Shindo Akihiro, Nishikawa Masakatsu, Niwa Atsushi, Sasaki Ryogen, Shindo Akihiro, Tomimoto Hidekazu, Murata Hiroto, Yata Kenichiro, Matsuo Koushun, Yagi Hideo, Shiogai Toshiyuki, Nagakane Yoshinari, Yamamoto Yasumasa, Fujinami Jun, Nakagawa Masanori, Ohara Ryo, Tomii Yasuhiro, Arakawa Yoshiki, Funaki Takeshi, Ihara Masafumi, Kitamura Akihiro, Maki Takakuni, Miyamoto Susumu, Nakaya Yoshifumi, Takahashi Ryosuke, Takenobu Yohei, Yoshida Kazumichi, Ino Tadashi, Murase Nagako, Ohotani Ryo, Tomii Yasuhiro, Yamamoto Yasumasa, Kawashima Atsushi, Watanabe Akiko, Hayashi Yuko, Ohmichi Takuma, Yasuda Rei, Yoshioka Akira, Yuki Natsuko, Makino Masahiro, Tomii Yasuhiro, Yamaguchi Tatsuyuki, Matsuzaki Jyo, Niki Hitoshi, Shiraishi Shoichi, Yanagihara Takehiko, Yamada Keiichi, Hatate Jun, Miwa Kaori, Okazaki Shuhei, Arihiro Shoji, Doijiri Ryosuke, Higashida Kyoko, Kajimoto Katsufumi, Miyashita Kotaro, Nagatsuka Kazuyuki, Saito Kozue, Sugiura Yuri, Takizawa Hotake, Torii Takako, Toyoda Kazunori, Yokota Chiaki, Kajimoto Yoshinaga, Kuroiwa Toshihiko, Fukunaga Ryuzo, Takahashi Tsutomu, Nakao Kazutami, Kajiyama Yuta, Kimura Yasuyoshi, Naka Takashi, Otomune Hironori, Tanahashi Takao, Uehara Takuya, Hashimoto Hiroyuki, Uematsu Toshihiko, Kataoka Kazuo, Okayama Satoshi, Somekawa Satoshi, Yamada Shuichi, Sasaki Rie, Yamano Shigeru, Nakao Naoyuki, Obayashi Shinji, Hamaguchi Hirotoshi, Toda Tatsushi, Washida Kazuo, Hoshi Taku, Kono Tomoyuki, Sekiya Hiroaki, Sugo Norifumi, Todo Kenichi, Togo Masaya, Yamagami Hiroshi, Yamamoto Shiro, Shiro Yoshihiko, Sugo Norifumi, Hamaguchi Hirotoshi, Takaoka Toshio, Abe Satoshi, Hamada Chizuko, Ishihara Masaki, Kadota Katuhiko, Nakagawa Tomonori, Oguro Hiroaki, Takayoshi Hiroyuki, Yamaguchi Takuya, Yamaguchi Shuuhei, Mizuhara Ryo, Okada Kazunori, Yamagata Shingo, Okada Kazunori, Sasaki Akira, Abe Koji, Deguchi Kentaro, Deguchi Shoko, Nakano Yumiko, Hirai Satoshi, Uno Masaaki, Yokosuka Kimihiko, Manabe Yasuhiro, Ito Hijiri, Aoki Shiro, Hosomi Naohisa, Kihara Yasuki, Kisaka Tomohiko, Maruyama Hirofumi, Matsumoto Masayasu, Araki Hayato, Ogami Ryo, Torii Tsuyoshi, Yokoyama Noboru, Yokoyama Takakazu, Kataoka Satoshi, Kitamura Takeshi, Kanda Takashi, Maeda Toshihiko, Shimizu Fumitaka, Seki Kozaburo, Bando Yuko, Ohara Masaki, Yamasaki Masahiro, Masahira Noritaka, Ueba Tetsuya, Ueba Yusuke, Sunami Norio, Fujimoto Yuichi, Haro Keiko, Ogata Hidenori, Shida Norihiko, Matsumoto Takeshi, Okamoto Kensho, Higaki Jitsuo, Okura Takafumi, Kawamoto Ryuichi, Arakawa Shuji, Arihiro Shoji, Shii Hirofumi, Kanai Hidetoshi, Fujimoto Shigeru, Jinnouchi Juro, Matsuki Takayuki, Osaki Masato, Arakawa Kimika, Ibaraki Ai, Kiyohara Kanako, Ohta Yuko, Oniki Hideyuki, Sakaki Minako, Tominaga Mitsuhiro, Tsuchihashi Takuya, Higashi Saho, Ishikawa Hiromi, Ishitsuka Koji, Kitayama Jiro, Nakane Hiroshi, Yoshimura Takeo, Kakino Shunsuke, Kaneko Yoshirou, Inoue Junnosuke, Maruyama Yoshikazu, Isa Katsunori, Ohya Yusuke, Sakima Hirokuni, Nakada Seigo

    JAMA NEUROLOGY   Vol. 76 ( 11 ) page: 1309 - 1318   2019.11

  30. Physiological Glucagon Acts as a Guardian of the Heart Against Catecholamine Surge Induced by Pressure-Overload

    Nishimura Kazuyuki, Bando Yasuko K., Kamihara Takahiro, Ozaki Reina, Yasheng Remina, Murohara Toyoaki

    CIRCULATION   Vol. 138   2018.11

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  31. Werner syndrome gene mutation is responsible for cardiac aging with transition from diastolic to systolic LV dysfunction

    Kamihara T. K., Bando Y. Kureishi, Nishimura K. N., Yasheng R. Y., Murohara T. M.

    EUROPEAN HEART JOURNAL   Vol. 39   page: 1398 - 1398   2018.8

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  32. Glucagon acts as a guardian of the heart against catecholamine surge

    Nishimura K. N., Bando Y. Kureishi, Kamihara T. K., Yasheng R. Y., Murohara T. M.

    EUROPEAN HEART JOURNAL   Vol. 39   page: 285 - 285   2018.8

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  33. Remote ischemic preconditioning protects human neural stem cells from oxidative stress

    Motomura Ayako, Shimizu Mikiko, Kato Akira, Motomura Kazuya, Yamamichi Akane, Koyama Hiroko, Ohka Fumiharu, Nishikawa Tomohide, Nishimura Yusuke, Hara Masahito, Fukuda Tetsuya, Bando Yasuhiko, Nishimura Toshihide, Wakabayashi Toshihiko, Natsume Atsushi

    APOPTOSIS   Vol. 22 ( 11 ) page: 1353 - 1361   2017.11

  34. The Selvester QRS score as a predictor of cardiac events in nonischemic dilated cardiomyopathy

    Hiraiwa H., Okumura T., Sawamura A., Sugiura Y., Kondo T., Watanabe N., Aoki S., Ichii T., Kano N., Fukaya K., Furusawa K., Morimoto R., Takeshita K., Bando Y., Murohara T.

    EUROPEAN HEART JOURNAL   Vol. 38   page: 143-144   2017.8

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  35. Metabolomic impact of glucagon-like peptide-1 on diabetic myocardium - glucagon-like peptide-1 accelerates myocardial glycolysis and utilizes more lactate as myocardial substrate

    Kawase H. K., Nishimura K. N., Yasheng R. Y., Bando Y. Kureishi, Murohara T.

    EUROPEAN HEART JOURNAL   Vol. 38   page: 338 - 338   2017.8

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  36. Is the administration of mineralocorticoid receptor antagonist required in asymptomatic AHA/ACC stage B heart failure patients?

    Okumura T., Sawamura A., Sugiura Y., Hiraiwa H., Kondo T., Aoki S., Watanabe N., Kano N., Fukaya K., Morimoto R., Bando Y. K., Murohara T.

    EUROPEAN HEART JOURNAL   Vol. 38   page: 698 - 698   2017.8

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  37. Abnormal Circadian Blood Pressure Profile as a Prognostic Marker in Patients with Nonischemic Dilated Cardiomyopathy

    Sawamura Akinori, Okumura Takahiro, Takeshita Kyosuke, Watanabe Naoki, Kano Naoaki, Mori Hiroaki, Fukaya Kenji, Morimoto Ryota, Hirashiki Akihiro, Bando Yasuko Kureishi, Murohara Toyoaki

    CARDIOLOGY   Vol. 136 ( 1 ) page: 1 - 9   2017

  38. Angiotensin type 1 receptor blocker reduces intimal neovascularization and plaque growth in apolipoprotein e-deficient mice Reviewed

    1. Cheng XW, Song H, Sasaki T, Hu L, Inoue A, Bando YK, Shi GP, Kuzuya M, Okumura K, Murohara T

    Hypertension   Vol. 57   page: 981-989   2011

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  39. Association of diabetes mellitus with myocardial collagen accumulation and relaxation impairment in patients with dilated cardiomyopath Reviewed

    Diabetes Res Clin Pract     page: 000-000   2011

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  40. Pitavastatin, an HMG-CoA reductase inhibitor, ameliorates endothelial function in chronic smokers. Reviewed

    Yoshida O, Kondo T, Kureishi-Bando Y, Sugiura T, Maeda K, Okumura K, Murohara T.

    Circ J   Vol. 74 ( 1 ) page: 195-202   2010.1

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    BACKGROUND: Smoking is a major cardiovascular risk factor, leading to endothelial dysfunction. The present study investigated the hypothesis that pitavastatin, an HMG-CoA reductase inhibitor, may improve endothelial function in chronic smokers via its antioxidant properties. METHODS AND RESULTS: The 30 male chronic smokers who exhibited mild hypercholesterolemia at the time of physical check-up were enrolled and randomized to the pitavastatin group (2 mg/day, n=15) or the untreated control group (n=15). Before and after the 4-week treatment period, endothelium-dependent flow-mediated dilation (FMD) and endothelium-independent dilation by glyceryl trinitrate (GTD) were examined, and the FMD/GTD ratio was calculated. The pitavastatin group showed a significant restoration of endothelial function (percent change in FMD: +49.6% vs +1.4%; percent change in FMD/GTD ratio: +26.6% vs 4.5%, P<0.05 respectively), and a significant reduction in oxidative stress levels (malondialdehyde-low-density lipoprotein-cholesterol: 16.6% vs +7.5%; free radical activity: 1.8% vs +9.7%, P<0.05 respectively) compared with the control group. Pitavastatin had no effect on the number of circulating CD34(+)CD133(+) progenitor cells, endothelial progenitor cells, or the MMP-2, MMP-9 and VEGF levels. In vitro oxidative stress monitoring assay revealed that pitavastatin protected endothelial cells against oxidative stress. CONCLUSIONS: Pitavastatin restores endothelial function, even in chronic smokers, possibly through its antioxidative properties.

  41. Atorvastatin prevents ischemic limb loss in type 2 diabetes: Role of p53. Reviewed

    J Atheroscl Thromb   Vol. 18   page: 200-208   2010

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  42. Optical coherence tomography images of a coronary artery aneurysm in an infarct related artery 6 months post bare-metal stent implantation Reviewed

    Yoshikawa D, Ishii H, Aoyama Y, Ichimiya H, Shimizu Y, Isobe S, Shintani S, Kureishi-Bando Y, Murohara T

    J Am Coll Cardiol Intv   Vol. 3   page: 1300-1302   2010

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  43. *Nifedipine Improves Endothelial Function. Role of Endothelial Progenitor Cells. Reviewed

    Sugiura T, Kondo T, Kureishi-Bando Y, Numaguchi Y, Yoshida O, Dohi Y, Kimura G,Ueda R, Rabelink TJ, Murohara T.

      Vol. 52   page: 1-8   2008.7

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  44. Heat shock-induced augmentation of vascular contractility is independent of rho-kinase. Reviewed

    Seok Y, Kim JI, Ito M, Kureishi Y, Nakano T, Kim SO, Lim DG, Park WH, Kim I.

    Clin Exp Pharmacol Physiol   Vol. 33 ( 3 ) page: 264-268   2006.3

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  45. Rho/Rho-kinase pathway contributes to C-reactive protein-induced plasminogen activator inhibitor-1 expression in endothelial cells. Reviewed

    Nakakuki T, Ito M, Iwasaki H, Kureishi Y, Okamoto R, Moriki N, Kongo M, Kato S, Yamada N, Isaka N, Nakano T.

    Arterioscler Thromb Vasc Biol.   Vol. 25 ( 10 ) page: 2088-2093   2005.10

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  46. The pro- and antiangiogenic effects of statins. Invited Reviewed

    Skaletz-Rorowski A, Kureishi Y, Shiojima I, Walsh K.

    Semin Vasc Med   Vol. 4 ( 4 ) page: 395-400   2005.5

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  47. Activation of PI3K-Akt pathway mediates antiapoptotic effects of beta-adrenergic agonist in airway eosinophils. Reviewed

    Machida K, Inoue H, Matsumoto K, Tsuda M, Fukuyama S, Koto H, Aizawa H, Kureishi Y, Hara N, Nakanishi Y.

    Am J Physiol Lung Cell Mol Physiol.   Vol. 288 ( 5 ) page: L860-867   2005.5

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  48. RhoA activation in vascular smooth muscle cells from stroke-prone spontaneously hypertensive rats. Reviewed

    Moriki N, Ito M, Seko T, Kureishi Y, Okamoto R, Nakakuki T, Kongo M, Isaka N, Kaibuchi K, Nakano T.

    Hypertens Res.   Vol. 27 ( 4 ) page: 263-270   2004.4

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  49. Akt and Ca2+ signaling in endothelial cells. Reviewed

    Ozeki M, Watanabe H, Luo J, Nakano T, Takeuchi K, Kureishi Y, Ito M, Nakano T, Ohashi K, Hayashi H.

      Vol. 259 ( 1-2 ) page: 169-170   2004.4

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  50. Activation of RhoA and inhibition of myosin phosphatase as important components in hypertension in vascular smooth muscle. Reviewed

    Seko T, Ito M, Kureishi Y, Okamoto R, Moriki N, Onishi K, Isaka N, Hartshorne DJ, Nakano T.

    Circ Res.   Vol. 92 ( 4 ) page: 411-418   2003.3

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  51. HMG-CoA reductase inhibitors promote cholesterol-dependent Akt/PKB translocation to membrane domains in endothelial cells. Reviewed

    Skaletz-Rorowski A, Lutchman M, Kureishi Y, Lefer DJ, Faust JR, Walsh K.

    Cardiovasc Res   Vol. 57 ( 10 ) page: 253-264   2003.1

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  52. Akt signaling mediates VEGF/VPF vascular permeability in vivo. Reviewed

    Six I, Kureishi Y, Luo Z, Walsh K.

    FEBS Lett   Vol. 532 ( 1-2 ) page: 67-69   2002.12

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  53. Regulation of angiogenesis by glycogen synthase kinase-3beta. Reviewed

    Kim HS, Skurk C, Thomas SR, Bialik A, Suhara T, Kureishi Y, Birnbaum M,Keaney JF Jr, Walsh K.

    J Biol Chem   Vol. 277 ( 44 ) page: 41888-41896   2002.11

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  54. Akt signaling mediates postnatal heart growth in response to insulin and nutritional status. Reviewed

    Shiojima I, Yefremashvili M, Luo Z, Kureishi Y, Takahashi A, Tao J,Rosenzweig A, Kahn CR, Abel ED, Walsh K.

    J Biol Chem   Vol. 277 ( 40 ) page: 37670-37677   2002.10

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  55. *Myogenic Akt signaling regulates blood vessel recruitment during myofiber growth. Reviewed

    Takahashi A, Kureishi Y, Yang J, Luo Z, Guo K, Mukhopadhyay D, IvashchenkoY, Branellec D, Walsh K.

    Mol Cell Biol.   Vol. 22 ( 13 ) page: 4803-4814   2002.7

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  56. Arachidonic acid-induced Ca2+ sensitization of smooth muscle contraction through activation of Rho-kinase. Reviewed

    Araki S, Ito M, Kureishi Y, Feng J, Machida H, Isaka N, Amano M, Kaibuchi K, Hartshorne DJ, Nakano T.

    Pflugers Arch   Vol. 441   page: 596-603   2001.11

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  57. HMG-CoA reductase inhibitor mobilizes bone marrow-derived endothelial progenitor cells. Reviewed

    Llevadot J, Murasawa S, Kureishi Y, Uchida S, Masuda H, Kawamoto A, Walsh K,

    J Clin Invest.   Vol. 108 ( 3 ) page: 399-405   2001.8

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  58. Akt down-regulation of p38 signaling provides a novel mechanism of vascular endothelial growth factor-mediated cytoprotection in endothelial cells. Reviewed

    Gratton JP, Morales-Ruiz M, Kureishi Y, Fulton D, Walsh K, Sessa WC.

    J Biol Chem   Vol. 276 ( 32 ) page: 30359-30365   2001.8

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  59. Activated Akt protects the lung from oxidant-induced injury and delays death of mice. Reviewed

    Lu Y, Parkyn L, Otterbein L, Kureishi Y, Walsh K, Ray A, Ray P.

    J. Exp. Med   Vol. 193   page: 545-549   2001

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  60. Akt1/PKB upregulation leads to vascular smooth muscle cell hypertrophy and polyploidization. Reviewed

    Hixon ML, Muro-Cacho C, Wagner MW, Obejero-Paz C, Millie E, Fujio Y, Kureishi Y, Hassold T, Walsh K, Gualberto A.

    J Clin Invest.   Vol. 106 ( 8 ) page: 1011-1020   2000.10

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  61. *The HMG-CoA reductase inhibitor simvastatin activates the protein kinase Akt and promotes angiogenesis in normocholesterolemic animals. Reviewed

    Kureishi Y, Luo Z, Shiojima I, Bialik A, Fulton D, Lefer DJ, Sessa WC, Walsh K.

    Nat Med.   Vol. 6 ( 9 ) page: 1004-1010   2000.9

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  62. *Acute modulation of endothelial Akt/PKB activity alters nitric oxide-dependent vasomotor activity in vivo. Reviewed

    Luo Z, Fujio Y, Kureishi Y, Rudic RD, Daumerie G, Fulton D, Sessa WC, Walsh K.

    J Clin Invest.   Vol. 106 ( 4 ) page: 493-499   2000.8

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  63. Regulation of smooth muscle cell migration and integrin expression by the Gax transcription factor. Reviewed

    Witzenbichler B, Kureishi Y, Luo Z, Le Roux A, Branellec D, Walsh K.

    J Clin Invest.   Vol. 104 ( 10 ) page: 1469-1480   1999.11

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  64. Regulation of Ca2+-independent smooth muscle contraction by alternative staurosporine-sensitive kinase. Reviewed

    Kureishi Y, Ito M, Feng J, Okinaka T, Isaka N, Nakano T.

    Eur J Pharmacol.   Vol. 376 ( 3 ) page: 315-320   1999.7

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    Authorship:Lead author   Language:English   Publishing type:Research paper (scientific journal)  

  65. Rho-associated kinase of chicken gizzard smooth muscle. Reviewed

    Feng J, Ito M, Kureishi Y, Ichikawa K, Amano M, Isaka N, Okawa K, Iwamatsu A, Kaibuchi K, Hartshorne DJ, Nakano T.

    J Biol Chem.   Vol. 274 ( 6 ) page: 3744-3752   1999.2

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    Language:English   Publishing type:Research paper (scientific journal)  

  66. Myosin light chain phosphorylation and contractile proteins in a canine two-hemorrhage model of subarachnoid hemorrhage. Reviewed

    Sun H, Kanamaru K, Ito M, Suzuki H, Kojima T, Waga S, Kureishi Y, Nakano T.

    Stroke.   Vol. 29 ( 10 ) page: 2139-2154   1998.10

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    Language:English   Publishing type:Research paper (scientific journal)  

  67. Expression, reconstitution and characterization of prolixin-S as a vasodilator--a salivary gland nitric-oxide-binding hemoprotein of Rhodnius prolixus.

    Yuda M, Higuchi K, Sun J, Kureishi Y, Ito M, Chinzei Y.

    Eur J Biochem.   Vol. 249 ( 1 ) page: 337-342   1997.10

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    Language:English   Publishing type:Research paper (scientific journal)  

  68. *Rho-associated kinase directly induces smooth muscle contraction through myosin light chain phosphorylation. Reviewed

    Kureishi Y, Kobayashi S, Amano M, Kimura K, Kanaide H, Nakano T, Kaibuchi K, Ito M.

    J Biol Chem.   Vol. 272 ( 19 ) page: 12257-12260   1997.5

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    Authorship:Lead author   Language:English   Publishing type:Research paper (scientific journal)  

  69. The relaxant effect of adrenomedullin on particular smooth muscles despite a general expression of its mRNA in smooth muscle, endothelial and epithelial cells. Reviewed

    Nishimura J, Seguchi H, Sakihara C, Kureishi Y, Yoshimura H, Kobayashi S, Kanaide H.

    Br J Pharmacol.   Vol. 120 ( 2 ) page: 193-200   1997.1

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    Language:English   Publishing type:Research paper (scientific journal)  

  70. Adrenomedullin decreases both cytosolic Ca2+ concentration and Ca(2+)-sensitivity in pig coronary arterial smooth muscle. Reviewed

    Kureishi Y, Kobayashi S, Nishimura J, Nakano T, Kanaide H.

    Biochem Biophys Res Commun.   Vol. 212 ( 2 ) page: 572-579   1995.7

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    Authorship:Lead author   Language:English   Publishing type:Research paper (scientific journal)  

  71. Modulation of smooth muscle calponin by protein kinase C and calmodulin. Reviewed

    Naka M, Kureishi Y, Muroga Y, Takahashi K, Ito M, Tanaka T.

    Biochem Biophys Res Commun.   Vol. 171 ( 3 ) page: 933-937   1990.9

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    Language:English   Publishing type:Research paper (scientific journal)  

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MISC 1

  1. A case of reexpansion pulmonary edema and acute pulmonary thromboembolism associated with diffuse large B-cell lymphoma treated with venovenous extracorporeal membrane oxygenation.

    Kazama S, Hiraiwa H, Kimura Y, Ozaki R, Shibata N, Arao Y, Oishi H, Kato H, Kuwayama T, Yamaguchi S, Kondo T, Furusawa K, Morimoto R, Okumura T, Bando YK, Sato T, Shimada K, Kiyoi H, Nakamura G, Yasuda Y, Kasugai D, Ogawa H, Higashi M, Yamamoto T, Jingushi N, Ozaki M, Numaguchi A, Goto Y, Matsuda N, Murohara T

    Journal of cardiology cases   Vol. 23 ( 1 ) page: 53 - 56   2021.1

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    Language:English   Publisher:Journal of Cardiology Cases  

    A 37-year-old man diagnosed with diffuse large B-cell lymphoma two weeks previously, visited our emergency department with sudden dyspnea. He had a severe respiratory failure with saturated percutaneous oxygen at 80% (room air). Chest radiography showed a large amount of left pleural effusion. After 1000 mL of the effusion was urgently drained, reexpansion pulmonary edema (RPE) occurred. Despite ventilator management, oxygenation did not improve and venovenous extracorporeal membrane oxygenation (VV-ECMO) was initiated in the intensive care unit. The next day, contrast-enhanced computed tomography showed a massive thrombus in the right pulmonary artery, at this point the presence of pulmonary thromboembolism (PTE) was revealed. Fortunately, the patient's condition gradually improved with anticoagulant therapy and VV-ECMO support. VV-ECMO was successfully discontinued on day 4, and chemotherapy was initiated on day 8. We speculated the following mechanism in this case: blood flow to the right lung significantly reduced due to acute massive PTE, and blood flow to the left lung correspondingly increased, which could have caused RPE in the left lung. Therefore, our observations suggest that drainage of pleural effusion when contralateral blood flow is impaired due to acute PTE may increase the risk of RPE. <Learning objective: This is a case of reexpansion pulmonary edema (RPE) in the left lung following acute pulmonary thromboembolism (PTE) in the right lung associated with malignant lymphoma, managed by venovenous extracorporeal membrane oxygenation. Contralateral pleural drainage could increase the risk of RPE because contralateral pulmonary blood flow is assumed to increase when PTE obstructs blood flow. Pleural drainage should be performed carefully in patients with malignant tumors because PTE may be hidden.>

    DOI: 10.1016/j.jccase.2020.08.013

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    PubMed

Presentations 7

  1. Localization of DPP4 in heart and its role in cardiac remodeling in pressure-overload heart failure. International conference

    Toshimasa Shigeta MD, Yasuko K Bando MD, PhD, Akio Monji MD, Xiang-wu Cheng MD, PhD, Toyoaki Murohara MD, PhD, FAHA

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    Event date: 2011.8

    Language:English   Presentation type:Poster presentation  

    Country:France  

  2. Activation of DPP4 promotes impaired coronary angiogenesis leading to myocardial ischemia in diabetic heart.

    Toshimasa Shigeta MD, Yasuko K Bando MD, PhD, Akio Monji MD, Xiang-wu Cheng MD, PhD, Toyoaki Murohara MD, PhD, FAHA

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    Event date: 2011.8

    Language:English   Presentation type:Oral presentation (general)  

    Country:Japan  

  3. Carolic restriction restores mitochondrial degeneration and cardiac remodeling in diabetic heart: Role of mitophagy.

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    Event date: 2011.8

    Language:English   Presentation type:Oral presentation (general)  

    Country:Japan  

  4. P53 controls cardiac insulin resistance and metabolic remodeling through AMPK in diabetic heart.

    Toshimasa Shigeta MD, Yasuko K Bando MD, PhD, Akio Monji MD, Xiang-wu Cheng MD, PhD, Toyoaki Murohara MD, PhD, FAHA

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    Event date: 2011.8

    Language:English   Presentation type:Oral presentation (general)  

    Country:Japan  

  5. 糖尿病性心筋障害におけるdipeptidyl peptidase (DPP4)の役割

    坂東泰子 重田寿正 室原豊明

    日本炎症・再生医学会 

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    Event date: 2011.6

    Language:Japanese   Presentation type:Poster presentation  

    Venue:京都   Country:Japan  

  6. たばこと血管の老化:喫煙による血管内皮傷害のメカニズム

    坂東泰子

    第11回日本抗加齢医学会 

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    Event date: 2011.5

    Language:Japanese   Presentation type:Symposium, workshop panel (nominated)  

    Venue:京都   Country:Japan  

  7. Hyperinsulinemia inhibits cardiac autophagy through the AMPK-mTOR pathway and enhances cardiac insulin resistance by p53 accumulation.

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    Event date: 2010.3

    Language:English   Presentation type:Oral presentation (general)  

    Country:Japan  

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Research Project for Joint Research, Competitive Funding, etc. 3

  1. 免疫チェックポイント阻害薬の安全な使用に資するirAE心筋障害スクリーニ ング手法と危険因子の探索研究

    Grant number:20lk0201123h0001  2020.10

    革新的がん医療実用化研究事業 

    田村雄一

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    Authorship:Coinvestigator(s)  Grant type:Competitive

    Grant amount:\390000 ( Direct Cost: \300000 、 Indirect Cost:\90000 )

  2. 心不全の発症予防をめざす治療薬及び診断マーカーの開発

    2012.11 - 2013.11

    AS242Z00997Q 

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    Grant type:Competitive

  3. Regulatory and diagnostic role of XXXX in XXXX of the heart

    2012.10

    Cooperative Research within Japan 

KAKENHI (Grants-in-Aid for Scientific Research) 7

  1. Glucagon-dependent autonomic regulatory system and its role in cardiovascular disease

    Grant number:19H03651  2019.4 - 2022.3

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    Authorship:Principal investigator 

    Grant amount:\16380000 ( Direct Cost: \12600000 、 Indirect Cost:\3780000 )

  2. グルカゴン関連蛋白と毛細血管機能にフォーカスした糖尿病性心筋症の病態に関する研究

    Grant number:18H02805  2018.4 - 2021.3

    室原 豊明

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    糖尿病合併心血管病の基本病態は血管障害であり、それらは大血管障害と毛細血管障害に分けられる。毛細血管障害については、予後や患者のQOLに悪影響をもたらすものの、未だに明確な病態が明らかにされておらず治療法も確立されていない。本研究では糖尿病性細小血管傷害による心機能の低下対して、特にインクレチンやグルカゴンと、毛細血管機能、血管新生機能に着目してその病態解明と新しい治療法の開発を目指す。血管新生因子、アディポカイン・マイオカインとの関連性についても検討する。
    (1)グルカゴン、GLP-1 研究
    グルカゴン関連ペプチド (glucagon, GLP-1, GIPなど) は、心筋細胞や血管内皮細胞にも受容体が存在し、直接的効果がある。近年グルカゴン関連ペプチドにより、血管新生を惹起できることが報告されており、グルカゴン関連ペプチドと糖尿病性毛細血管障害の関連性が注目されている。大規模臨床試験でもGLP-1受容体作動薬が心血管イベントを有意に低下させることが示され、その機序について注目が集まっている。我々はグルカゴン・GLP-1欠損マウスを入手し研究を継続した。その結果興味ある知見を得たので、論文投稿中である。
    (2)アディポカイン・マイオカイン研究
    我々のグループはこれまでに新規アディポカイン・マイオカインを複数同定しており、これらが虚血部血管新生作用を有していることもまた報告した。2018年度には新規マイオカインの1つであるマイオネクチンを同定し、その生物学的特性に関して論文発表を行った(Otaka N. et al. Circ. Res. 2018;123:1326-1338.)。心筋虚血再灌流モデルマウスにおいて、マイオネクチンは心筋保護作用を示した。マイオネクチンは運動により骨格筋からの分泌が増強する。これらの研究を現在継続中である。
    アディポカイン・マイオカイン研究においては、新規マイオカインの1つであるマイオネクチンを同定し、その生物学的特性に関して解析を行った(Otaka N. et al. Circ. Res. 2018;123:1326-1338.)。この延長として、心筋梗塞の一般的な動物モデルである、心筋虚血再灌流モデルマウスにおいて、マイオネクチンは心筋保護作用を示した。またマイオネクチンは運動により骨格筋からの分泌が増強することから、非常に興味深い分子である。これらのデータを現在投稿準備中である。
    また、グルカゴン関連ペプチド (glucagon, GLP-1, GIPなど) に関連する研究では、我々はグルカゴン・GLP-1欠損マウスを入手する事が出来て、研究を継続している。糖尿病性心機能障害や毛細血管障害に対するグルカゴン関連ペプチドの役割について研究継続中である。現在は論文作成を終えて、海外雑誌に投稿中である。また学会でもデータを発表している(Nishimura et al. Glucagon acts as a guardian of the heart against catecholamine elevation. 2019年3月 日本循環器学会総会にて発表)。
    引き続き、グルカゴン関連ペプチド(グルカゴンとGLP-1)欠損マウスを用い、心筋虚血モデル、TAC 心不全モデル、血管新生モデルなどを用いて、グルカゴンや GLP-1受容体作動薬剤の心血管系に与える役割を検討して行きたい。また、アディポカイン、マイオカインについても、引き続き動脈硬化モデル、血管新生モデル、心不全モデルなどの動物モデルを用いて、それらの効果を検討して行きたい。
    2020年度から新たに当科において、肺高血圧症モデルマウスを作成する予定である。このモデルにおける血管新生と病態、さらにはグルカゴン関連ペプチド、アディポカイン、マイオカインの効果を見て行きたい。

  3. Pathophysiological significance of the Klotho-FGF system in myocardial diseases

    Grant number:16K09429  2016.4 - 2020.3

    Okumura Takahiro

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    We examined the relationship between serum FGF-23 levels and biomarkers, hemodynamics, and prognosis in 42 patients with dilated cardiomyopathy. FGF-23 levels in peripheral vein was negatively correlated with estimated glomerular filtration rate and positively with high-sensitivity troponin T levels. In survival analysis, the cardiac event rate was significantly higher in the High FGF-23 group than in the Low FGF-23 group. In multivariate analysis, the high FGF-23 group was an independent predictor of cardiac events. In multiple regression analysis, the estimated glomerular filtration rate and brain natriuretic peptide levels were significant determinants of FGF-23 levels. Collagen volume fraction in endomyocardial biopsy samples was not significantly correlated with peripheral FGF-23 levels, but was weakly correlated with the transcardiac gradient of FGF-23 levels defined as the difference in concentration between the coronary sinus and the base of the aorta.

  4. Role of aging regulatory protein WRN in cardiac fibrosis

    Grant number:16K09496  2016.4 - 2019.3

    Bando Yasuko K.

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    Authorship:Principal investigator 

    Grant amount:\4680000 ( Direct Cost: \3600000 、 Indirect Cost:\1080000 )

    [Background/Introduction] Aging is known to be one of the primary causes of heart failure. Werner syndrome is one of the aging disorder that caused by dysfunction of DNA helicase-regulatory protein (WRN). [Results] WRN-K577M exhibited diffuse left-ventricular (LV) hypertrophy, enhanced fibrosis, and diastolic LV
    dysfunction with preserved systolic ejection fraction. DNA microarray analysis of WRN-K577M heart revealed that the 253 genes were upregulated including hypertrophy, fibrosis, inflammation, and oxidative stress. Notably, p62 and LC3-II/I were increased in myocardium of WRN-K577M. Blockade of the lysosomal fusion into autophagosome by systemic treatment with chloroquine reduced LC3-II/I ratio.[Conclusion(s)] In WRN-mutant progeria model, off-rate disorder of cardiac autophagy is, at least in part, the cause of increase in oxidative stress and inflammation in heart leading to HFpEF.

  5. Mechanism of GLP 1 / DDP4 in stress vascular disease and its therapeutic application

    Grant number:15H04802  2015.4 - 2018.3

    Cheng XianWU

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    Authorship:Coinvestigator(s) 

    Exposure to psychosocial stress is a risk factor for cardiovascular disease. Here, we have used dipeptidyl peptidase-4 (DPP4)-deficient mice and its inhibitor as well as glucagon-like peptide-1 (GLP-1) receptor agonist to explore the role of DPP4/GLP-1 axis in ischemia-induced neovascularization and diet-induced atherosclerosis. We demonstrated that stress impaired the recovery of the ischemic/normal blood-flow ratio throughout the follow-up period and capillary formation; and these changes DPP4 inhibition and GLP-1R activation improved these changes; these benefits were abrogated by adiponectin blocking and genetic depletion. Similarly, chronic stress accelerated diet-induced atherosclerotic lesion formation; and this effect was reversed by DPP4 inhibition. Our findings suggest that CatK might be a new therapeutic target for the chronic psychological stress-related neovascularization and cardiovascular diseases.

  6. 心不全における新たな病態制御機構の解明:セリンプロテアーゼDPP4の役割

    2011.4 - 2013.3

    科学研究費補助金  基盤研究(C)

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    Authorship:Principal investigator 

  7. Mechanisms of vasculopathy underlying diabetic cardiomyopathy and development of novel therapeutic strategy.

    2008.4 - 2010.3

    Grant-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research(A)

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    Authorship:Coinvestigator(s) 

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Industrial property rights 1

  1. 微小血管障害又はその関連疾患のバイオマーカー

    重田寿正, 室原豊明

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    Application no:2010-236964  Date applied:2010.10

    Patent/Registration no:6065172  Date registered:2017.1 

    Country of applicant:Domestic  

 

Social Contribution 1

  1. 日本禁煙科学会学術集会

    Role(s):Presenter, Lecturer, Planner, Organizing member

    日本禁煙科学会  日本禁煙科学会学術集会 in 愛知  2018.10

Media Coverage 1

  1. 心臓の老化を止める

    ABC  たけしの家庭の医学  2019.4

Academic Activities 7

  1. 日本循環器学会BCVR学術総会

    Role(s):Planning, management, etc., Panel moderator, session chair, etc., Review, evaluation, Peer review

    日本循環器学会BCVR学術総会  2020.9

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    Type:Competition, symposium, etc. 

  2. 日本臨床腫瘍学会ガイドライン作成委員

    Role(s):Planning, management, etc., Planning/Implementing academic research

    2020.4

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    Type:Academic society, research group, etc. 

  3. 日本循環器学会ダイバーシティ委員会部会長

    Role(s):Planning, management, etc.

    日本循環器学会ダイバーシティ委員会  2020.4

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    Type:Academic society, research group, etc. 

  4. 日本循環器学会IT/Database部会 International contribution

    Role(s):Planning, management, etc., Planning/Implementing academic research, Peer review

    日本循環器学会IT/Database部会  2020.4

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    Type:Academic society, research group, etc. 

  5. 日本循環器学会BCVR部会

    Role(s):Planning, management, etc.

    日本循環器学会BCVR部会  2020.4

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    Type:Academic society, research group, etc. 

  6. 腫瘍循環器ハンドブック編集委員会幹事

    Role(s):Planning, management, etc., Supervision (editorial), Peer review

    日本腫瘍循環器学会  2020.2 - 2020.12

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    Type:Academic society, research group, etc. 

  7. ISHR日本部会 International contribution

    Role(s):Planning, management, etc.

    ISHR日本部会  2019.4

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