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Review
. 2020 Sep 4;21(18):6483.
doi: 10.3390/ijms21186483.

Vitamin D and Cardiovascular Disease, with Emphasis on Hypertension, Atherosclerosis, and Heart Failure

Affiliations
Review

Vitamin D and Cardiovascular Disease, with Emphasis on Hypertension, Atherosclerosis, and Heart Failure

Nejla Latic et al. Int J Mol Sci. .

Abstract

Vitamin D deficiency is the most common nutritional deficiency, affecting almost one billion people worldwide. Vitamin D is mostly known for its role in intestinal calcium absorption and bone mineralization. However, the observation of seasonal changes in blood pressure and the subsequent identification of vitamin D receptor (VDR) and 1α-hydroxylase in cardiomyocytes, as well as endothelial and vascular smooth muscle cells, implicated a role of vitamin D in the cardiovascular system. Animal studies provided compelling evidence that vitamin D signaling is essential for cardiovascular integrity, especially for the regulation of vascular tone and as an antifibrotic and antihypertrophic signaling pathway in the heart. In addition, observational studies reported an association between vitamin D deficiency and risk of hypertension, atherosclerosis, and heart failure. However, recent clinical intervention studies failed to prove the causal relationship between vitamin D supplementation and beneficial effects on cardiovascular health. In this review, we aim to highlight our current understanding of the role of vitamin D in the cardiovascular system and to find potential explanations for the large discrepancies between the outcome of experimental studies and clinical intervention trials.

Keywords: atherosclerosis; cardiovascular disease; endothelial dysfunction; heart failure; hypertension; vitamin D.

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Conflict of interest statement

The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results.

Figures

Figure 1
Figure 1
Biological effects of vitamin D signaling in vitamin D receptor (VDR)-expressing target cells are determined by the sum of circulating 1,25(OH)2D concentrations in addition to locally produced 1,25(OH)2D. The 1,25(OH)2D3–VDR complex dimerizes with the retinoid X receptor (RXR) and translocates to the nucleus where it binds to vitamin D response elements (VDRE) found in the promoter region of target genes. 25(OH)D originating from the blood stream can be locally converted into 1,25(OH)2D in cells expressing 1α-hydroxylase.

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