Journal
CURRENT PHARMACEUTICAL DESIGN
Volume 12, Issue 12, Pages 1543-1547Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/138161206776389877
Keywords
advanced glycation end products; atherosclerosis; diabetes; insulin resistance; nitric oxide; oxidative stress
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Impaired endothelial cell (EC) growth and function have been proposed to be an initial event that leads to the development of atherosclerosis. There is a growing body of evidence that atherosclerosis is an inflammatory-fibroproliferative disease, and ECs are target for cytokines and growth factors released during inflammation. Recently, nifedipine, one of the most widely used dihydropyridine-based calcium antagonists (DHPs) for treatments of patients with hypertension, was shown to inhibit vascular inflammation and subsequently improve endothelial function in many cardiovascular diseases, thus slowing the development and progression of atherosclerosis. However, the molecular mechanisms underlying this are not fully understood, because ECs do not possess voltage-operated L-type calcium channels. In this review, we discuss the pleiotropic effects of nifedipine on atherosclerosis, especially focusing on its anti-oxidative properties.
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