Peroxisome Proliferator-Activated Receptor γ and Cardiovascular Diseases

Abstract

Peroxisome proliferator-activated receptors (PPARs) are members of the nuclear receptor superfamily and form heterodimers with retinoid X receptor. Three PPAR isoforms have been isolated and termed α, β (or δ) and γ. Although PPARγ is expressed predominantly in adipose tissue and associated with adipocyte differentiation and glucose homeostasis, PPARγ is also present in a variety of cell types. Synthetic antidiabetic thiazolidinediones (TZDs) are well known as ligands and activators for PPARγ. After it was reported that activation of PPARγ suppressed production of pro-inflammatory cytokines in activated macrophages, medical interest in PPARγ has grown and there has been a huge research effort. PPARγ is currently known to be implicated in various human chronic diseases such as diabetes mellitus, atherosclerosis, rheumatoid arthritis, inflammatory bowel disease, and Alzheimer's disease. Many studies suggest that TZDs not only ameliorate insulin sensitivity, but also have pleiotropic effects on many tissues and cell types. Although activation of PPARγ seems to have beneficial effects on cardiovascular diseases, the mechanisms by which PPARγ ligands prevent their development are not fully understood. Recent data about the actions and its mechanisms of PPARγ-dependent pathway in cardiovascular diseases are discussed here. (Circ J 2009; 73: 214 - 220)