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Peroxisome Proliferator-Activated Receptor-β and its Agonists in Hypertension and Atherosclerosis

Peroxisome Proliferator-Activated Receptor-β and its Agonists in Hypertension and Atherosclerosis Cardiovascular diseases are the leading cause of morbidity and mortality in the US. Proper management and/ or prevention of atherosclerosis and hypertension, two complex and chronic disorders, would significantly reduce the risk for cardiovascular events such as myocardial infarction and stroke, but this requires an understanding of the mechanisms underlying their development and progression. Whereas a great deal has been learned and applied toward the management of these disorders, especially hypertension, morbidity and mortality remains unacceptably high, most likely because there are disease-causing mechanisms that have yet to be fully recognized. Understanding these disease mechanisms is necessary so that novel management strategies can be developed. One of these novel mechanisms centers on peroxisome proliferator-activated receptor (PPAR)-β. PPAR-β is a member of the nuclear receptor superfamily of ligand-activated transcription factors known to play a role in glucose homeostasis and adipocyte differentiation and, more recently, has been shown to have anti-inflammatory, antiatherogenic, and antihypertensive effects. Thiazolidinediones, a class of drugs used in the treatment of type 2 diabetes mellitus, are high-affinity ligands for PPAR-β. In this review, the anti-inflammatory, anti-atherosclerotic, and anti-hypertensive mechanisms by which PPAR-β and its agonists are thought to exert protective effects on the cardiovascular system are discussed. Ongoing clinical trials using PPAR-β activators for the management of cardiovascular diseases, especially in patients with type 2 diabetes mellitus, are summarized. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png American Journal of Cardiovascular Drugs Springer Journals

Peroxisome Proliferator-Activated Receptor-β and its Agonists in Hypertension and Atherosclerosis

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References (97)

Publisher
Springer Journals
Copyright
Copyright © 2005 by Adis Data Information BV
Subject
Medicine & Public Health; Cardiology; Pharmacotherapy; Pharmacology/Toxicology
ISSN
1175-3277
eISSN
1179-187X
DOI
10.2165/00129784-200505060-00006
pmid
16259527
Publisher site
See Article on Publisher Site

Abstract

Cardiovascular diseases are the leading cause of morbidity and mortality in the US. Proper management and/ or prevention of atherosclerosis and hypertension, two complex and chronic disorders, would significantly reduce the risk for cardiovascular events such as myocardial infarction and stroke, but this requires an understanding of the mechanisms underlying their development and progression. Whereas a great deal has been learned and applied toward the management of these disorders, especially hypertension, morbidity and mortality remains unacceptably high, most likely because there are disease-causing mechanisms that have yet to be fully recognized. Understanding these disease mechanisms is necessary so that novel management strategies can be developed. One of these novel mechanisms centers on peroxisome proliferator-activated receptor (PPAR)-β. PPAR-β is a member of the nuclear receptor superfamily of ligand-activated transcription factors known to play a role in glucose homeostasis and adipocyte differentiation and, more recently, has been shown to have anti-inflammatory, antiatherogenic, and antihypertensive effects. Thiazolidinediones, a class of drugs used in the treatment of type 2 diabetes mellitus, are high-affinity ligands for PPAR-β. In this review, the anti-inflammatory, anti-atherosclerotic, and anti-hypertensive mechanisms by which PPAR-β and its agonists are thought to exert protective effects on the cardiovascular system are discussed. Ongoing clinical trials using PPAR-β activators for the management of cardiovascular diseases, especially in patients with type 2 diabetes mellitus, are summarized.

Journal

American Journal of Cardiovascular DrugsSpringer Journals

Published: Aug 20, 2012

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