A Review on Vitamin D Deficiency and Risk of Cardiovascular Disease

Abstract

Calcium and phosphorus metabolism are regulated by vitamin D in skeletal health. Nonskeletal tissues also produce vitamin D metabolites, which influence regulatory pathways via paracrine and autocrine mechanisms. One of vitamin D’s active metabolites, 1,25-dihydroxyvitamin D (1,25(OH)2 D), binds to the vitamin D receptor and regulates numerous genes that may play a role in heart disease, including cell proliferation, differentiation, apoptosis, oxidative stress, membrane transport, matrix homeostasis, and adhesion. It has been discovered that all kinds of cardiovascular cells, such as cardiomyocytes, arterial wall cells, and immune cells, contain vitamin D receptors (VDRs). Inflammation, thrombosis, and the renin-angiotensin system are all affected by vitamin D metabolites, according to experimental studies. Various manifestations of degenerative cardiovascular disease (CVD), such as vascular calcification, have been associated with vitamin D deficiency in clinical studies. However, vitamin D supplementation has yet to be proven as a means of managing CVD. The purpose of this review is to summarize clinical studies that show associations between vitamin D status and CVD as well as experimental studies exploring the mechanisms underlying these associations.