Vitamin D3, or cholecalciferol, is a secosteroid hormone that is either consumed in the diet or generated de novo through the interaction of ultraviolet light with precursor sterols in the basal layers of the epidermis. The vitamin D receptor (VDR) and ligand-generating 1α (OH)ase are found throughout the cardiovascular tree and appear to be regulated by physiologically (and pathophysiologically) relevant stimuli. The liganded VDR promotes vasorelaxation through effects in the vascular endothelium. It also inhibits angiogenesis and suppresses vascular inflammation. The VDR plays an important role in maintaining the integrity of cardiac structure. Lack of VDR signaling leads to cardiac hypertrophy and fibrosis. Cardiac abnormalities induced by vitamin D deficiency can be reversed by treatment with 1,25(OH)2D3and its less hypercalcemic analogs. 25(OH)D3deficiency has been linked to a variety of cardiovascular (as well as noncardiovascular) diseases including hypertension, peripheral arterial disease (PAD), and heart failure. However, studies carried out to date have not demonstrated a clear beneficial role for vitamin D, its metabolites, or analogs in managing these disorders. Clinical trials designed to address these questions are planned or under way. © 2011 Elsevier Inc. All rights reserved.
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