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Peroxisome proliferator‐activated receptors in the cardiovascular system
Author(s) -
BishopBailey David
Publication year - 2000
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0703149
Subject(s) - nuclear receptor , peroxisome proliferator activated receptor , receptor , peroxisome , peroxisome proliferator activated receptor gamma , peroxisome proliferator activated receptor alpha , peroxisome proliferator activated receptor delta , biology , fibrate , endocrinology , medicine , microbiology and biotechnology , biochemistry , transcription factor , cholesterol , gene
Peroxisome proliferator‐activated receptor (PPAR)s are a family of three nuclear hormone receptors, PPARα, ‐δ, and ‐γ, which are members of the steriod receptor superfamily. The first member of the family (PPARα) was originally discovered as the mediator by which a number of xenobiotic drugs cause peroxisome proliferation in the liver. Defined functions for all these receptors, until recently, mainly concerned their ability to regulate energy balance, with PPARα being involved in β‐oxidation pathways, and PPARγ in the differentiation of adipocytes. Little is known about the functions of PPARδ, though it is the most ubiquitously expressed. Since their discovery, PPARs have been shown to be expressed in monocytes/macrophages, the heart, vascular smooth muscle cells, endothelial cells, and in atherosclerotic lesions. Furthermore, PPARs can be activated by a vast number of compounds including synthetic drugs, of the clofibrate, and anti‐diabetic thiazoldinedione classes, polyunsaturated fatty acids, and a number of eicosanoids, including prostaglandins, lipoxygenase products, and oxidized low density lipoprotein. This review will aim to introduce the field of PPAR nuclear hormone receptors, and discuss the discovery and actions of PPARs in the cardiovascular system, as well as the source of potential ligands. British Journal of Pharmacology (2000) 129 , 823–834; doi: 10.1038/sj.bjp.0703149