Adipose‐derived protein omentin prevents neointimal formation after arterial injury

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

doi:10.1096/fj.14-258129

Cited by 58 publications

(36 citation statements)

References 34 publications

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“…Omentin also attenuates the inflammatory response to TNF in cultured vascular endothelial cells via AMPK/eNOS-mediated signaling 77) . Furthermore, we have demonstrated that transgenic mice expressing omentin in fat tissue show reduced neointimal formation in response to injury in vivo 78) . Omentin suppresses growth of vascular smooth muscle cells through an AMPK-dependent mechanism.…”

Section: Resultsmentioning

confidence: 90%

Adipocytokines in Cardiovascular and Metabolic Diseases

Ouchi

2016

JAT

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Obesity, particularly excess visceral fat accumulation, is highly associated with the development of metabolic syndrome and atherosclerotic cardiovascular disease. Adipose tissue produces a variety of secreted proteins, referred to as adipocytokines, which directly affect nearby or remote organs. Dysregulation of adipocytokines caused by obese conditions contributes to the pathogenesis of various metabolic and cardiovascular disorders. This review focuses on the significance of several adipocytokines that potentially exert beneficial actions on obesity-related diseases, including atherosclerosis and ischemic heart disease.J Atheroscler Thromb, 2016; 23: 645-654.

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Section: Resultsmentioning

confidence: 90%

Adipocytokines in Cardiovascular and Metabolic Diseases

Ouchi

2016

JAT

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“…Furthermore, systemic delivery of omentin-1 attenuated neointimal thickening and vascular cell proliferation in the injured arteries of mice. 63 Omentin-1 reduces the growth of vascular smooth muscle cells in an AMPK-dependent mechanism (Figure 3). Transgenic overexpression of omentin-1 reduces neointimal formation in response to injury, accompanied by attenuated inflammatory response in injured vessels.…”

Section: Ctrp9mentioning

confidence: 99%

Role of Adipokines in Cardiovascular Disease

Lau

Ohashi

Wang

et al. 2017

Circ J

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Cardiovascular disease (CVD) is the greatest cause of death, accounting for nearly one-third of all deaths worldwide. The increase in obesity rates over 3 decades is widespread and threatens the public health in both developed and developing countries. Obesity, the excessive accumulation of visceral fat, causes the clustering of metabolic disorders, such as type 2 diabetes, dyslipidemia, and hypertension, culminating in the development of CVD. Adipose tissue is not only an energy storage organ, but an active endocrine tissue producing various biologically active proteins known as adipokines. Since leptin, a central regulator of food intake and energy expenditure, was demonstrated to be an adipose-specific adipokine, attention has focused on the identification and characterization of unknown adipokines to clarify the mechanisms underlying obesity-related disorders. Numerous adipokines have been identified in the past 2 decades; most adipokines are upregulated in the obese state. Adipokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β, and resistin are pro-inflammatory, and exacerbate various metabolic and cardiovascular diseases. However, a small number of adipokines, including adiponectin, are decreased by obesity, and generally exhibit antiinflammatory properties and protective functions against obesity-related diseases. Collectively, an imbalance in the production of pro-and antiinflammatory adipokines in the obese condition results in multiple complications. In this review, we focus on the pathophysiologic roles of adipokines with cardiovascular protective properties.

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“…In addition, omentin-1 has been suggested to increase AMPactivated protein kinase (AMPK) phosphorylation, and to promote endothelial cell function e.g. enhancement of endothelial cell differentiation [32], protection of cardiac myocytes from apoptosis during ischemia [33] and attenuate neointimal formation after arterial injury in vivo [34]. Furthermore, omentin-1 may exert antiinflammatory functions via AMPK signaling pathway [35e37].…”

Section: Groupmentioning

confidence: 99%