Abstract
Peroxisome proliferator-activated receptors (PPARs) are transcription factors belonging to a nuclear receptor superfamily. PPARs have three isoforms: α, β (or δ), and γ. It is known that PPARγ is expressed predominantly in adipose tissue and promotes adipocyte differentiation and glucose homeostasis. Recently, synthetic antidiabetic thiazolidinediones (TZDs) and the natural prostaglandin D 2 (PGD 2) metabolite, 15-deoxy-Δ 12,14-prostaglandin J 2 (15d-PGJ 2), have been identified as ligands for PPARγ. Furthermore, it has become apparent that PPARs are present both in a variety of different cell types and in atherosclerotic lesions and the studies about PPARγ have been extended. Although activation of PPARγ appears to have protective effects on atherosclerosis, it is still largely uncertain whether PPARγ ligands prevent the development of cardiovascular disease. Recent evidence suggests that some benefit from antidiabetic agents, TZDs, may occur independent of increased insulin sensitivity. In this article, we review the latest developments in the PPAR field and summarize the roles of PPARγ and the actions of PPARγ ligands in the cardiovascular system.
Published Version
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