Key result
Adipokines act as crucial mediators linking obesity with atherosclerosis by regulating lipid accumulation, inflammation, and endothelial function.
Adipokines serve as key molecular links between obesity and atherosclerosis, offering potential novel therapeutic targets for cardiovascular disease.
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Adipokine modulation remains investigational for obesity-related atherosclerosis; leaves open clinical utility pending prospective trials.
Atherosclerotic cardiovascular disease is a major health problem around the world. Obesity is a primary risk factor for atherosclerosis and is associated with increased morbidity and mortality of cardiovascular diseases. However, the precise molecular pathways underlying this close association remain poorly understood. Adipokines are cytokines, chemokines and hormones secreted by adipose tissue that couple the regulation of lipid accumulation, inflammation, and atherogenesis, and therefore serve to link obesity with cardiovascular disorders. Obesity-related disorders including metabolic syndrome, diabetes, atherosclerosis, hypertension, and coronary artery disease are associated with dysregulated adipokine(s) expression. Recent studies demonstrate the proinflammatory effects as well as atherogenic properties of adipokines. Adipokines also participate in the regulation of endothelial function, which is an early event in atherosclerosis. By contrast, adiponectin, an adipocyte-derived hormone, exerts anti-inflammatory, anti-atherogenic and vascular protective effects. Furthermore, there is an interactive association among adipokines, by which adipokines reciprocally regulate each other's expression. Understanding this interplay may reveal plausible mechanisms for treating atherosclerosis and coronary heart disease by modulating adipokine(s) expression. In this review, we discuss insights into the role and the therapeutic potential of adipokines as mediators of atherosclerosis.
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Hanrui Zhang (2010) conducted a review in Atherosclerosis. Adipokines was evaluated. Adipokines act as crucial mediators linking obesity with atherosclerosis by regulating lipid accumulation, inflammation, and endothelial function.
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