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Journal of Pharmacology and Toxicology
  Year: 2007 | Volume: 2 | Issue: 3 | Page No.: 205-219
DOI: 10.3923/jpt.2007.205.219
 
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Peroxisome Proliferator Activated Receptor Agonists: Emerging Therapy for Cardiovascular Complications

Pitchai Balakumar, Madhankumar Rose and Manjeet Singh

Abstract:
Peroxisome Proliferator Activated Receptors (PPARs) are ligand-activated transcription factors of nuclear hormone receptor superfamily. The PPAR subfamily comprises of three members such as PPARα, PPARγ and PPARδ. Activation of PPARα induces gene expressions that promote fatty acid oxidation. Fibrates, which are currently used as hypolipidemic agents are PPARα ligands. PPARγ regulates gene expressions that promote insulin sensitization followed by glucose metabolism. Thiazolidinediones, which are presently employed as insulin-sensitizing anti-diabetic agents are PPARγ agonists. On the other hand, PPARδ also known as PPARβ is expressed ubiquitously and involved in fatty acid oxidation in tissues, which lack PPARα. But no selective PPARδ agonists are currently available for therapeutic use. Evidences from ongoing pre-clinical and clinical studies suggest that PPAR ligands exert broad spectrum of cardioprotective activities in addition to their above-mentioned properties. Agonists of PPARs are shown to inhibit the pathogenesis of atherosclerosis, endothelial dysfunction, heart failure and myocardial infarction. In this review, we discussed various recently developed PPAR ligands and their potential role in the prevention of pathogenesis of cardiovascular complications. Moreover, the novel class of currently developed PPAR dual agonists such as PPARα/γ and PPARα/δ agonists and pan agonists such as PPARα/γ/δ agonists have also been discussed, which may be novel emerging therapeutic agents for cardiovascular complications.
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How to cite this article:

Pitchai Balakumar, Madhankumar Rose and Manjeet Singh, 2007. Peroxisome Proliferator Activated Receptor Agonists: Emerging Therapy for Cardiovascular Complications. Journal of Pharmacology and Toxicology, 2: 205-219.

DOI: 10.3923/jpt.2007.205.219

URL: https://scialert.net/abstract/?doi=jpt.2007.205.219

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