Peroxisome Proliferator-Activated Receptor γ and Cardiovascular Diseases

被引:64
|
作者
Takano, Hiroyuki [1 ]
Komuro, Issei [1 ]
机构
[1] Chiba Univ, Grad Sch Med, Dept Cardiovasc Sci & Med, Chuo Ku, Chiba 2608670, Japan
关键词
Atherosclerosis; Cardiac hypertrophy; Heart failure; PPAR-gamma; Thiazolidinedione; CORONARY-ARTERY-DISEASE; SMOOTH-MUSCLE-CELLS; PPAR-GAMMA; GENE-EXPRESSION; ANGIOTENSIN-II; CARDIAC-HYPERTROPHY; IN-VITRO; CHOLESTEROL EFFLUX; ENDOTHELIAL-CELLS; FLUID RETENTION;
D O I
10.1253/circj.CJ-08-1071
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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 alpha, beta (or delta) and gamma. Although PPAR gamma is expressed predominantly in adipose tissue and associated with adipocyte differentiation and a glucose homeostasis, PPAR gamma is also present in a variety of cell types. Synthetic antidiabetic thiazolidinediones (TZDs) are well known as ligands and activators for PPAR gamma. After it was reported that activation of PPAR gamma suppressed production of pro-inflammatory cytokines in activated macrophages, medical interest in PPAR gamma has grown and there has been a huge research effort. PPAR gamma 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 PPAR), seems to have beneficial effects on cardiovascular diseases, the mechanisms by which PPAR gamma ligands prevent their development are not fully understood. Recent data about the actions and its mechanisms of PPAR gamma-dependent pathway in cardiovascular diseases are discussed here. (Circ J 2009;73:214-220)
引用
收藏
页码:214 / 220
页数:7
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