Vitamin D Therapy in Cardiac Hypertrophy and Heart Failure.

Curr Pharm Des. 2011 Jun 1.
Wu-Wong JR.
Department of Pharmacy Practice University of Illinois at Chicago 833 South Wood Street Chicago, IL. 60612-7230, USA. jrwuwong@uic.edu.

Vitamin D(3) is made in the skin, modified in the liver to form 25(OH)D, and then further hydroxylated in the kidney to form the active hormone, 1,25-dihydroxyvitamin D(3) (calcitriol). Calcitriol binds to and activates the vitamin D receptor (VDR), a nuclear receptor, to regulate numerous downstream signaling pathways in different cells and tissues.

Is Emerging evidence suggests that VDR plays an important role in modulating cardiovascular, immunological, metabolic and other functions. Data from preclinical, epidemiological and clinical studies have shown that deficiency in VDR activation is associated with an increased risk for cardiovascular disease (CVD).

Results from interventional trials using either nutritional vitamin D or VDR agonists (VDRAs), support the idea that VDR activation is beneficial for improving the underlying factors of CVD such as *hypertension,

• endothelial dysfunction,
• atherosclerosis,
• vascular calcification,
• cardiac hypertrophy and
• progressive renal dysfunction.

Furthermore, a majority of chronic kidney disease (CKD) patients die of CVD and VDRA therapy is associated with a survival benefit in both pre-dialysis and dialysis CKD patients.

Most of the studies measured serum 25(OH)D as an indication for vitamin D deficiency, which does not truly reflect the VDR activation status. Although VDR plays an important role in regulating cardiovascular function and VDRAs may be potentially useful for treating CVD, at pre sent VDRAs are not indicated for the treatment of CVD.

PMID: 21631423
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