Circulation Research. 2005;96:939-949
doi: 10.1161/01.RES.0000163635.62927.34
doi: 10.1161/01.RES.0000163635.62927.34
© 2005 American Heart Association, Inc.
Reviews |
Adipose Tissue, Inflammation, and Cardiovascular Disease
From the Departments of Cell Biology (A.H.B., P.E.S.), Medicine (P.E.S.), Division of Endocrinology, and Diabetes Research and Training Center (P.E.S.), Albert Einstein College of Medicine, Bronx, NY. A.H. Berg’s present address: Department of Pathology, Brigham and Women’s Hospital, 75 Francis St, Boston, MA 02115.
Correspondence to Philipp E. Scherer, Albert Einstein College of Medicine 1300 Morris Park Ave, Bronx, NY 10461. E-mail scherer{at}aecom.yu.edu
This Review is part of a thematic series on Adipocyte Signaling in the Cardiovascular System, which includes the following articles:
Adipose Tissue, Inflammation, and Cardiovascular Disease
Diabetic Cardiomyopathy
Adipocyte Signaling and Lipid Homeostasis
Adipocyte Signaling and the Vasculature
PPAR
Activation and Effects on the Vasculature
Philipp E. Scherer Guest Editor
Mounting evidence highlights the role of adipose tissue in the development of a systemic inflammatory state that contributes to obesity-associated vasculopathy and cardiovascular risk. Circulating mediators of inflammation participate in the mechanisms of vascular insult and atheromatous change, and many of these inflammatory proteins are secreted directly from adipocytes and adipose tissue–derived macrophages. Several factors linking obesity with an increased cardiovascular risk have been identified. The adipocyte-specific secretory protein adiponectin is a particularly promising candidate in this context. Its levels are decreased in obesity. Adiponectin may mediate some of its demonstrated cardioprotective effects through its anti-inflammatory properties. In addition to decreased expression of beneficial adipokines, secretion of a host of inflammatory factors from visceral adipose tissue may contribute to the increased cardiovascular risk associated with obesity. The cardioprotective effects of many of the most popular drug regimens corroborate these conclusions, demonstrating that along with improvements in other therapeutic end points, they mediate improvements in systemic inflammation. In some cases, these improvements are attributable to direct suppression of inflammatory signaling in adipocytes. The targeted suppression of various proinflammatory cascades in adipocytes specifically represents an exciting new therapeutic opportunity for the cardiovascular disease area.
Key Words: adipocyte • secretion • inflammation
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