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Interplay between statins and PPARs in improving cardiovascular outcomes: a double‐edged sword?
Author(s) -
Balakumar Pitchai,
Mahadevan Nanjaian
Publication year - 2012
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 - 10.1111/j.1476-5381.2011.01597.x
Subject(s) - medicine , cholesterol , hmg coa reductase , pharmacology , inflammation , bioinformatics , reductase , statin , biology , enzyme , biochemistry
Statins are best‐selling medications in the management of high cholesterol and associated cardiovascular complications. They inhibit 3‐hydroxy‐3‐methylglutaryl‐coenzyme A (HMG‐CoA)‐reductase in order to prevent disproportionate cholesterol synthesis. Statins slow the progression of atherosclerosis, prevent the secondary cardiovascular events and improve the cardiovascular outcomes in patients with elevated cholesterol levels. The underlying mechanisms pertaining to the cardioprotective role of statins are linked with numerous pleiotropic actions including inhibition of inflammatory events and improvement of endothelial function, besides an effective cholesterol‐lowering ability. Intriguingly, recent studies suggest possible interplay between statins and nuclear transcription factors like PPARs, which should also be taken into consideration while analysing the potential of statins in the management of cardiovascular complications. It could be suggested that statins have two major roles: (i) a well‐established cholesterol‐lowering effect through inhibition of HMG‐CoA‐reductase; (ii) a newly explored PPAR‐activating property, which could mediate most of cardiovascular protective pleiotropic effects of statins including anti‐inflammatory, antioxidant and anti‐fibrotic properties. The present review addressed the underlying principles pertaining to the modulatory role of statins on PPARs.