Editorials |
From Molecular Cardiology/Whitaker Cardiovascular Institute, Boston University School of Medicine, Mass.
Correspondence to Kenneth Walsh, PhD, Molecular Cardiology/Whitaker Cardiovascular Institute Boston University School of Medicine 715 Albany Street, W611 Boston, MA 02118. E-mail kxwalsh@bu.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Accumulating evidence indicates that chronic inflammation linked to obesity is closely associated with the development of diabetes and cardiovascular disorders.1 The inflammatory marker C-reactive protein (CRP) has been shown to be an independent predictor of future risk for cardiovascular events and a risk factor of developing diabetes.2,3 High levels of CRP are also associated with obesity and coronary heart disease,4,5 suggesting that CRP is a useful biomarker for obesity-linked chronic inflammatory states. Furthermore, although CRP is primarily made by liver, new studies have shown that CRP is also produced by diseased tissues (eg, atherosclerotic lesions) and by various cell types including macrophages, smooth muscle cells, and endothelial cells.6–8 Increasing evidence indicates that CRP is not just a biomarker of inflammation but that it has a direct proinflammatory action through its ability to promote the induction of cytokines.6 Thus, agents that lower CRP levels have clinical utility for treatment of inflammatory diseases.
See accompanying article on page 1368
A number of bioactive molecules secreted from fat tissue, referred to as adipokines, could participate in the development of obesity-related complications through regulation of inflammatory responses.9,10 Most adipokines are proinflammatory. In contrast, adiponectin, also referred to as adipocyte complement-related protein 30 (ACRP30), is an antiinflammatory adipokine that is abundantly present in blood stream. Whereas adiponectin is expressed almost exclusively in adipose tissue,11,12 plasma adiponectin levels are paradoxically decreased in obese individuals.13 This regulation of adiponectin results, at least in part, from the upregulation of tumor necrosis factor (TNF)-
and other proinflammatory cytokines which
Related Article:
Arterioscler Thromb Vasc Biol 2008 28: 1368-1374.
This article has been cited by other articles:
![]() |
D. J. Chess, R. J. Khairallah, K. M. O'Shea, W. Xu, and W. C. Stanley A high-fat diet increases adiposity but maintains mitochondrial oxidative enzymes without affecting development of heart failure with pressure overload Am J Physiol Heart Circ Physiol, November 1, 2009; 297(5): H1585 - H1593. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. Summer, C. A. Fiack, Y. Ikeda, K. Sato, D. Dwyer, N. Ouchi, A. Fine, H. W. Farber, and K. Walsh Adiponectin deficiency: a model of pulmonary hypertension associated with pulmonary vascular disease Am J Physiol Lung Cell Mol Physiol, September 1, 2009; 297(3): L432 - L438. [Abstract] [Full Text] [PDF] |
||||
|
ATVB Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2008 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |