Faculty Profiles - OHASHI, Koji

Papers - OHASHI, Koji

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Adipolin/CTRP12 protects against pathological vascular remodelling through suppression of smooth muscle cell growth and macrophage inflammatory response Reviewed

Hayato Ogawa, Koji Ohashi, Masanori Ito, Rei Shibata, Noriyoshi Kanemura, Daisuke Yuasa, Takahiro Kambara, Kazuhiro Matsuo, Satoko Hayakawa, Mizuho Hiramatsu-Ito, Naoya Otaka, Hiroshi Kawanishi, Shukuro Yamaguchi, Takashi Enomoto, Takaya Abe, Mari Kaneko, Mikito Takefuji, Toyoaki Murohara, Noriyuki Ouchi

Cardiovascular Research Vol. 116 ( 1 ) page： 237 - 249 2020.1

Language：Japanese Publishing type：Research paper (scientific journal) Publisher：Oxford University Press (OUP)

<title>Abstract</title>
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<title>Aims</title>
Secreted factors produced by adipose tissue are involved in the pathogenesis of cardiovascular disease. We previously identified adipolin, also known as C1q/TNF-related protein 12, as an insulin-sensitizing adipokine. However, the role of adipolin in vascular disease remains unknown. Here, we investigated whether adipolin modulates pathological vascular remodelling.

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<title>Methods and results</title>
Adipolin-knockout (APL-KO) and wild-type (WT) mice were subjected to wire-induced injury of the femoral artery. APL-KO mice showed increased neointimal thickening after vascular injury compared with WT mice, which was accompanied by an enhanced inflammatory response and vascular cell proliferation in injured arteries. Adipolin deficiency also led to a reduction in transforming growth factor-β (TGF-β) 1 protein levels in injured arteries. Treatment of cultured macrophages with adipolin protein led to a reduction in lipopolysaccharide-stimulated expression of inflammatory mediators, including tumour necrosis factor (TNF)-α, interleukin (IL) 6, and monocyte chemotactic protein (MCP)-1. These effects were reversed by inhibition of TGF-β receptor II (TGF-βRII)/Smad2 signalling. Adipolin also reduced platelet-derived growth factor (PDGF)-BB-stimulated proliferation of vascular smooth muscle cells (VSMCs) through a TGF-βRII/Smad2-dependent pathway. Furthermore, adipolin treatment significantly increased TGF-β1 concentration in media from cultured VSMCs and macrophages.

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<title>Conclusion</title>
These data indicate that adipolin protects against the development of pathological vascular remodelling by attenuating macrophage inflammatory responses and VSMC proliferation.

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DOI： 10.1093/cvr/cvz074

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Other Link： http://academic.oup.com/cardiovascres/article-pdf/116/1/237/31555893/cvz074.pdf

Protein Kinase N Promotes Stress-Induced Cardiac Dysfunction Through Phosphorylation of Myocardin-Related Transcription Factor A and Disruption of its Interaction with Actin. Reviewed

Sakaguchi T, Takefuji M, Wettschureck N, Hamaguchi T, Amano M, Kato K, Tsuda T, Eguchi S, Ishihama S, Mori Y, Yura Y, Yoshida T, Unno K, Okumura T, Ishii H, Shimizu Y, Bando YK, Ohashi K, Ouchi N, Enomoto A, Offermanns S, Kaibuchi K, Murohara T

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

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

Eguchi S, Takefuji M, Sakaguchi T, Ishihama S, Mori Y, Tsuda T, Takikawa T, Yoshida T, Ohashi K, Shimizu Y, Hayashida R, Kondo K, Bando YK, Ouchi N, Murohara T

The Journal of biological chemistry Vol. 294 ( 31 ) page： 11665 - 11674 2019.8

Associations among circulating levels of follistatin-like 1, clinical parameters, and cardiovascular events in patients undergoing elective percutaneous coronary intervention with drug-eluting stents. Reviewed

Aikawa T, Shimada K, Miyauchi K, Miyazaki T, Sai E, Ouchi S, Kadoguchi T, Kunimoto M, Joki Y, Dohi T, Okazaki S, Isoda K, Ohashi K, Murohara T, Ouchi N, Daida H

PloS one Vol. 14 ( 4 ) page： e0216297 2019.4

Myonectin Is an Exercise-Induced Myokine That Protects the Heart From Ischemia-Reperfusion Injury Reviewed

Otaka Naoya, Shibata Rei, Ohashi Koji, Uemura Yusuke, Kambara Takahiro, Enomoto Takashi, Ogawa Hayato, Ito Masanori, Kawanishi Hiroshi, Maruyama Sonomi, Joki Yusuke, Fujikawa Yusuke, Narita Shingo, Unno Kazumasa, Kawamoto Yoshiyuki, Murate Takashi, Murohara Toyoaki, Ouchi Noriyuki

CIRCULATION RESEARCH Vol. 123 ( 12 ) page： 1326-1338 2018.12

Role of Adipokines in Cardiovascular Disease Reviewed

Lau Wayne Bond, Ohashi Koji, Wang Yajing, Ogawa Hayato, Murohara Toyoaki, Ma Xin-Liang, Ouchi Noriyuki

CIRCULATION JOURNAL Vol. 81 ( 7 ) page： 920-928 2017.7

C1q/TNF-related protein 1 prevents neointimal formation after arterial injury Reviewed

Kanemura Noriyoshi, Shibata Rei, Ohashi Koji, Ogawa Hayato, Hiramatsu-Ito Mizuho, Enomoto Takashi, Yuasa Daisuke, Ito Masanori, Hayakawa Satoko, Otaka Naoya, Murohara Toyoaki, Ouchi Noriyuki

ATHEROSCLEROSIS Vol. 257 page： 138-145 2017.2

The role of adipokines in cardiovascular disease Reviewed

Shibata Rei, Ouchi Noriyuki, Ohashi Koji, Murohara Toyoaki

JOURNAL OF CARDIOLOGY Vol. 70 ( 3-4 ) page： 329-334 2017

Protective Roles of Adipocytokines and Myokines in Cardiovascular Disease Reviewed

Noriyuki Ouchi, Koji Ohashi, Rei Shibata, Toyoaki Murohara

CIRCULATION JOURNAL Vol. 80 ( 10 ) page： 2073 - 2080 2016.10

Language：Japanese Publishing type：Research paper (scientific journal) Publisher：JAPANESE CIRCULATION SOC

Obesity is a major risk factor for progression of cardiovascular disease. Adipose tissue is recognized as an endocrine organ producing various secretory molecules, also known as adipocytokines, and dysregulated production of adipocytokines participates in the pathogenesis of obesity complications, including metabolic dysfunction and cardiovascular disorders. Recent evidence indicates that skeletal muscle also functions as an endocrine organ capable of secreting a number of bioactive substances, also referred to as myokines. Several myokines are involved in metabolic and cardiovascular regulation. This review will discuss the clinical and experimental studies that have investigated the protective role of several adipocytokines and myokines in cardiovascular diseases.

DOI： 10.1253/circj.CJ-16-0663

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Association of Circulating Follistatin-Like 1 Levels with Inflammatory and Oxidative Stress Markers in Healthy Men Reviewed

Satoko Hayakawa, Koji Ohashi, Rei Shibata, Ryotaro Takahashi, Naoya Otaka, Hayato Ogawa, Masanori Ito, Noriyoshi Kanemura, Mizuho Hiramatsu-Ito, Nobuo Ikeda, Toyoaki Murohara, Noriyuki Ouchi

PLOS ONE Vol. 11 ( 5 ) page： e0153619 2016.5

Language：Japanese Publishing type：Research paper (scientific journal) Publisher：PUBLIC LIBRARY SCIENCE

Objectives
Follistatin-like 1 (Fstl1) is a circulating glycoprotein that plays a crucial role in cardiovascular diseases and inflammation-related disorders. We have shown that Fstl1 acts as an anti-inflammatory factor that protects against ischemic heart disease and chronic kidney disease. Here we examined whether plasma level of Fstl1 associates with markers of inflammation and oxidative stress in apparently healthy Japanese men.
Methods and Results
Plasma Fstl1 levels were measured by enzyme-linked immunosorbent assay. Circulating Fstl1 concentrations positively correlated with levels of fasting immune-reactive insulin (FIRI), high-sensitive CRP (hsCRP) and derivatives of reactive oxidative metabolites (dROMs), an indicator of oxidative stress. The levels of hsCRP positively associated with Fstl1, body mass index (BMI), triglyceride, FIRI and dROMs levels. dROMs levels positively associated with Fstl1, Hemoglobin A1c and hsCRP levels. Multiple regression analysis with confounding factors revealed that Fstl1 levels, together with BMI and FIRI, correlated with hsCRP and that Fstl1 levels correlated with dROMs.
Conclusion
Our observations indicate that measurement of plasma Fstl1 levels can be valuable for assessment of pro-inflammatory and oxidative stress conditions.

DOI： 10.1371/journal.pone.0153619

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Omentin attenuates atherosclerotic lesion formation in apolipoprotein E-deficient mice Reviewed

Mizuho Hiramatsu-Ito, Rei Shibata, Koji Ohashi, Yusuke Uemura, Noriyoshi Kanemura, Takahiro Kambara, Takashi Enomoto, Daisuke Yuasa, Kazuhiro Matsuo, Masanori Ito, Satoko Hayakawa, Hayato Ogawa, Naoya Otaka, Shinji Kihara, Toyoaki Murohara, Noriyuki Ouchi

CARDIOVASCULAR RESEARCH Vol. 110 ( 1 ) page： 107 - 117 2016.5

Language：Japanese Publishing type：Research paper (scientific journal) Publisher：OXFORD UNIV PRESS

Obesity is associated with the development of atherosclerosis. We previously demonstrated that omentin is a circulating adipokine that is downregulated in association with atherosclerotic diseases. Here, we examined the impact of omentin on the development of atherosclerosis with gain-of-function genetic manipulations and dissected its potential mechanism.
Apolipoprotein E-deficient (apoE-KO) mice were crossed with transgenic mice expressing the human omentin gene (OMT-Tg) mice in fat tissue to generate apoE-KO/OMT-Tg mice. ApoE-KO/OMT-Tg mice exhibited a significant reduction of the atherosclerotic areas in aortic sinus, compared with apoE-KO mice despite similar lipid levels. ApoE-KO/OMT-Tg mice also displayed significant decreases in macrophage accumulation and mRNA expression of proinflammatory mediators including tumour necrosis factor-alpha, interleukin-6, and monocyte chemotactic protein-1 in aorta when compared with apoE-KO mice. Treatment of human monocyte-derived macrophages with a physiological concentration of human omentin protein led to reduction of lipid droplets and cholesteryl ester content. Treatment with human omentin protein also reduced lipopolysaccharide-induced expression of proinflammatory genes in human macrophages. Treatment of human macrophages with omentin promoted the phosphorylation of Akt. Inhibition of Akt signalling abolished the anti-inflammatory actions of omentin in macrophages.
These data document for the first time that omentin reduces the development of atherosclerosis by reducing inflammatory response of macrophages through the Akt-dependent mechanisms.

DOI： 10.1093/cvr/cvv282

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C1q/TNF-related protein-1 functions to protect against acute ischemic injury in the heart Reviewed

Daisuke Yuasa, Koji Ohashi, Rei Shibata, Naoki Mizutani, Yoshiyuki Kataoka, Takahiro Kambara, Yusuke Uemura, Kazuhiro Matsuo, Noriyoshi Kanemura, Satoko Hayakawa, Mizuho Hiramatsu-Ito, Masanori Ito, Hayato Ogawa, Takashi Murate, Toyoaki Murohara, Noriyuki Ouchi

FASEB JOURNAL Vol. 30 ( 3 ) page： 1065 - 1075 2016.3

Language：Japanese Publishing type：Research paper (scientific journal) Publisher：FEDERATION AMER SOC EXP BIOL

Obesity is associated with an increased risk of cardiovascular disease. C1q/TNF-related protein (CTRP)-1 is a poorly characterized adipokine that is up-regulated in association with ischemic heart disease. We investigated the role of CTRP1 in myocardial ischemia injury. CTRP1-knockout mice showed increased myocardial infarct size, cardiomyocyte apoptosis, and proinflammatory gene expression after I/R compared with wild-type (WT) mice. In contrast, systemic delivery of CTRP1 attenuated myocardial damage after I/R in WT mice. Treatment of cardiomyocytes with CTRP1 led to reduction of hypoxia-reoxygenation-induced apoptosis and lipopolysaccharide-stimulated expression of proinflammatory cytokines, which was reversed by inhibition of sphingosine-1-phosphate (S1P) signaling. Treatment of cardiomyocytes with CTRP1 also resulted in the increased production of cAMP, which was blocked by suppression of S1P signaling. The antiapoptotic and anti-inflammatory actions of CTRP1 were cancelled by inhibition of adenylyl cyclase or knockdown of adiponectin receptor 1. Furthermore, blockade of S1P signaling reversed CTRP1-mediated inhibition of myocardial infarct size, apoptosis, and inflammation after I/R in vivo. These data indicate that CTRP1 protects against myocardial ischemic injury by reducing apoptosis and inflammatory response through activation of the S1P/cAMP signaling pathways in cardiomyocytes, suggesting that CTRP1 plays a crucial role in the pathogenesis of ischemic heart disease.

DOI： 10.1096/fj.15-279885

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Role of a novel secreted factor omentin in cardiovascular disease Reviewed

Ouchi Noriyuki, Ohashi Koji, Shibata Rei, Murohara Toyoaki

JOURNAL OF PHARMACOLOGICAL SCIENCES Vol. 128 ( 3 ) page： S35 - S35 2015.7

C1q/Tumor Necrosis Factor-Related Protein 9 Protects against Acute Myocardial Injury through an Adiponectin Receptor I-AMPK-Dependent Mechanism Reviewed

Takahiro Kambara, Rei Shibata, Koji Ohashi, Kazuhiro Matsuo, Mizuho Hiramatsu-Ito, Takashi Enomoto, Daisuke Yuasa, Masanori Ito, Satoko Hayakawa, Hayato Ogawa, Tamar Aprahamian, Kenneth Walsh, Toyoaki Murohara, Noriyuki Ouchi

MOLECULAR AND CELLULAR BIOLOGY Vol. 35 ( 12 ) page： 2173 - 2185 2015.6

Language：Japanese Publishing type：Research paper (scientific journal) Publisher：AMER SOC MICROBIOLOGY

Obesity is a risk factor for cardiovascular disease. C1q/tumor necrosis factor-related protein 9 (CTRP9) is an adipokine that is downregulated by obesity. We investigated the role of CTRP9 in cardiac injury with loss-of-function genetic manipulations and defined the receptor-mediated signaling pathway downstream of this adipokine. CTRP9-knockout (CTRP9-KO) mice at the age of 12 weeks were indistinguishable from wild-type (WT) mice under basal conditions. CTRP9-KO mice had exacerbated contractile left ventricle dysfunction following intraperitoneal injection of lipopolysaccharide (LPS) compared to WT mice. Administration of LPS to CTRP9-KO mice also resulted in increased expression of proinflammatory cytokines and oxidative stress markers in the heart compared to WT mice. Likewise, CTRP9-KO mice showed increased myocardial infarct size and elevated expression of inflammatory mediators in ischemic heart following ischemia and reperfusion compared to WT mice. Treatment of cardiac myocytes with CTRP9 protein led to suppression of LPS-induced expression of proinflammatory genes, which was reversed by blockade of AMPK or ablation of adiponectin receptor I (AdipoR1). Systemic delivery of CTRP9 attenuated LPS-induced cardiac dysfunction in WT mice but not in muscle-specific transgenic mice expressing dominant-negative mutant form of AMPK or in AdipoR1-knockout mice. CTRP9 protects against acute cardiac damage in response to pathological stimuli by suppressing inflammatory reactions through AdipoR1/AMPK-dependent mechanisms.

DOI： 10.1128/MCB.01518-14

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FGF21 attenuates pathological myocardial remodeling following myocardial infarction through the adiponectin-dependent mechanism Reviewed

Yusuke Joki, Koji Ohashi, Daisuke Yuasa, Rei Shibata, Masanori Ito, Kazuhiro Matsuo, Takahiro Kambara, Yusuke Uemura, Satoko Hayakawa, Mizuho Hiramatsu-Ito, Noriyoshi Kanemura, Hayato Ogawa, Hiroyuki Daida, Toyoaki Murohara, Noriyuki Ouchi

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS Vol. 459 ( 1 ) page： 124 - 130 2015.3

Language：Japanese Publishing type：Research paper (scientific journal) Publisher：ACADEMIC PRESS INC ELSEVIER SCIENCE

Ischemic heart disease is one of the leading causes of death. Fibroblast growth factor 21 (FGF21) is a circulating factor with an anti-diabetic property. Skeletal muscle is an important source of FGF21 production. Here, we investigated whether skeletal muscle-derived FGF21 modulates cardiac remodeling in a murine model of myocardial infarction. Myocardial infarction was produced in C57BL/6J wild-type (WT) mice by the permanent ligation of the left anterior descending coronary artery (LAD). Adenoviral vectors expressing FGF21 (Ad-FGF21) or control beta-galactosidase were intramuscularly injected into mice at 3 days before permanent LAD ligation. Intramuscular injection of Ad-FGF21 increased plasma FGF21 levels in WT mice compared with control. Treatment of WT mice with Ad-FGF21 led to improvement of left ventricular systolic dysfunction and dilatation at 2 weeks after LAD ligation. Ad-FGF21 administration to WT mice also led to enhancement of capillary density in the infarct border zone, and reduction of myocyte apoptosis in the remote zone, which were accompanied by decreased expression of pro-inflammatory cytokines. Furthermore, treatment of WT mice with Ad-FGF21 increased plasma levels of adiponectin, which is a cardioprotective adipokine. The beneficial effects of Ad-FGF21 on cardiac dysfunction and inflammatory response after myocardial infarction were diminished in adiponectin-knockout mice. These data suggest that muscle-derived FGF21 ameliorates adverse cardiac remodeling after myocardial infarction, at least in part, through an adiponectin-dependent mechanism. (C) 2015 Elsevier Inc. All rights reserved.

DOI： 10.1016/j.bbrc.2015.02.081

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Neuron-Derived Neurotrophic Factor Ameliorates Adverse Cardiac Remodeling After Experimental Myocardial Infarction. Reviewed

Joki Y, Ohashi K, Yuasa D, Shibata R, Kataoka Y, Kambara T, Uemura Y, Matsuo K, Hayakawa S, Hiramatsu-Ito M, Kanemura N, Ito M, Ogawa H, Daida H, Murohara T, Ouchi N.

Circulation: Heart Failure page： in press 2015.2

Omentin functions to attenuate cardiac hypertrophic response Reviewed

Kazuhiro Matsuo, Rei Shibata, Koji Ohashi, Takahiro Kambara, Yusuke Uemura, Mizuho Hiramatsu-Ito, Takashi Enomoto, Daisuke Yuasa, Yusuke Joki, Masanori Ito, Satoko Hayakawa, Hayato Ogawa, Shinji Kihara, Toyoaki Murohara, Noriyuki Ouchi

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY Vol. 79 page： 195 - 202 2015.2

Language：Japanese Publishing type：Research paper (scientific journal) Publisher：ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD

Cardiac hypertrophy occurs in many obesity-related conditions. Omentin is an adipose-derived plasma protein that is downregulated under obese conditions. Here, we investigated whether omentin modulates cardiac hypertrophic responses in vivo and in vitro. Systemic administration of an adenoviral vector expressing human omentin (Ad-OMT) to wild-type (WT) mice led to the attenuation of cardiac hypertrophy, fibrosis and ERK phosphorylation induced by transverse aortic constriction (TAC) or angiotensin II infusion. In cultured cardiomyocytes, stimulation with phenylephrine (PE) led to an increase in myocyte size, which was prevented by pretreatment with human omentin protein. Pretreatment of cardiomyocytes with omentin protein also reduced ERK phosphorylation in response to PE stimulation. Ad-OMT enhanced phosphorylation of AMP-activated protein kinase (AMPK) in the heart of WT mice after TAC operation. Blockade of AMPK activation by transduction with dominant-negative mutant forms of AMPK reversed the inhibitory effect of omentin on myocyte hypertrophy and ERK phosphorylation following PE stimulation. Moreover, fat-specific transgenic mice expressing human omentin showed reduced cardiac hypertrophy and ERK phosphorylation following TAC surgery compared to littermate controls. These data suggest that omentin functions to attenuate the pathological process of myocardial hypertrophy via the activation of AMPK in the heart, suggesting that omentin may represent a target molecule for the treatment of cardiac hypertrophy. (C) 2014 Elsevier Ltd. All rights reserved.

DOI： 10.1016/j.yjmcc.2014.11.019

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Adipose-derived protein omentin prevents neointimal formation after arterial injury Reviewed

Yusuke Uemura, Rei Shibata, Noriyoshi Kanemura, Koji Ohashi, Takahiro Kambara, Mizuho Hiramatsu-Ito, Takashi Enomoto, Daisuke Yuasa, Yusuke Joki, Kazuhiro Matsuo, Masanori Ito, Satoko Hayakawa, Hayato Ogawa, Toyoaki Murohara, Noriyuki Ouchi

FASEB JOURNAL Vol. 29 ( 1 ) page： 141 - 151 2015.1

Language：Japanese Publishing type：Research paper (scientific journal) Publisher：FEDERATION AMER SOC EXP BIOL

Obesity is highly linked with the development of vascular diseases. Omentin is a circulating adipokine that is downregulated in patients with cardiovascular diseases. In this study, we investigated the role of omentin in regulation of vascular remodeling in response to injury. Wild-type (WT) mice were treated intravenously with adenoviral vectors encoding human omentin (Ad-OMT) or control beta-gal and subjected to arterial wire injury. Ad-OMT treatment reduced the neointimal thickening and the frequencies of bromodeoxyuridine-positive proliferating cells in injured arteries. Treatment of vascular smooth muscle cells (VSMCs) with human omentin protein at a physiologic concentration led to suppression of growth and ERK phosphorylation after stimulation with various growth factors. Omentin stimulated AMPK signaling in VSMCs, and blockade of AMPK reversed omentin-mediated inhibition of VSMC growth and ERK phosphorylation. Furthermore, fat-specific human omentin transgenic (OMT-TG) mice exhibited reduced neointimal thickening and vascular cell growth following vascular injury. AMPK activation was enhanced in injured arteries in OMT-TG mice, and administration of AMPK inhibitor reversed the reduction of neointimal hyperplasia in OMT-TG mice. These data indicate that omentin attenuates neointimal formation after arterial injury and suppresses VSMC growth through AMPK-dependent mechanisms. Thus, omentin can represent a novel target molecule for the prevention of vascular disorders.

DOI： 10.1096/fj.14-258129

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Adiponectin as a Target in Obesity-related Inflammatory State Reviewed

Koji Ohashi, Daisuke Yuasa, Rei Shibata, Toyoaki Murohara, Noriyuki Ouchi

ENDOCRINE METABOLIC & IMMUNE DISORDERS-DRUG TARGETS Vol. 15 ( 2 ) page： 145 - 150 2015

Language：English Publishing type：Research paper (scientific journal) Publisher：BENTHAM SCIENCE PUBL LTD

Accumulating evidence indicates that low grade inflammation is closely associated with obesity-related disorders including type 2 diabetes, hypertension and atherosclerosis. Adiponectin is a fat-derived plasma protein with anti-inflammatory functions. Circulating levels of adiponectin are decreased in obese states, and these conditions are broadly associated with various obesity-related diseases. Furthermore, adiponectin has direct protective functions against cardiovascular disease, cerebrovascular disease, non-alcoholic steatohepatitis (NASH) and chronic kidney disease (CKD). In this review, we will focus on the protective functions of adiponectin against these obesity-related diseases from the view point of its anti-inflammatory properties.

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The potential of adipokines as therapeutic agents for cardiovascular disease Reviewed

Rei Shibata, Koji Ohashi, Toyoaki Murohara, Noriyuki Ouchi

CYTOKINE & GROWTH FACTOR REVIEWS Vol. 25 ( 4 ) page： 483 - 487 2014.8

Language：Japanese Publishing type：Research paper (scientific journal) Publisher：ELSEVIER SCI LTD

Adipose tissue functions as an endocrine organ by producing bioactive secretory proteins, also known as adipokines, that can directly act on nearby or remote organs. Most of the adipokines are upregulated by obese conditions, and typically promote obese complications. In contrast, some adipokines, such as adiponectin, CTRP9 and omentin, are downregulated in obese states. These factors exert salutary actions on obesity-linked cardiovascular disorders. In this review, we focus on the significance of adiponectin, CTRP9 and omentin as therapeutic agents for cardiovascular disease. (C) 2014 Elsevier Ltd. All rights reserved.

DOI： 10.1016/j.cytogfr.2014.07.005

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Papers - OHASHI, Koji