Abstract

Vitamin D represents a group of secosteroids involved in the calcium and phosphate metabolism. The active form of vitamin D, 1,25-dihydroxylcalciferol, exerts its biological mechanisms via the VDR (vitamin D receptor) which acts as a regulator of several target genes. Hypovitaminosis D is associated with many diseases, which are not only limited to the metabolism of the skeleton, but growing evidence links the deficit of vitamin D to cardiovascular, metabolic, immune, and neoplastic diseases. In regard to the cardiovascular system, current evidence shows the presence of VDR in endothelial cells. Moreover, both in vitro and animal experimental models demonstrated that the deficit of vitamin D can promote endothelial dysfunction and atherosclerosis development. Vitamin D can interfere with vascular functions also by affecting the production of vasodilator mediators. VDR is also expressed in left ventricle cardiomyocytes, and hypovitaminosis D can relate to cardiac hypertrophy and heart failure. Randomized clinical trials (RCT) designed to prove the therapeutic role of vitamin D supplementation have been inconclusive to date. The aim of this review is to highlight the main interactions between vitamin D metabolism and cardiovascular diseases; thus, focusing on pathogenic mechanisms and related clinical manifestations.

Highlights

  • Vitamin D is a group of secosteroids that physiologically improve the intestinal absorption of calcium and phosphate

  • Current in vivo evidence suggests that the loss of the activity of the vitamin D signaling pathway can induce the remodeling of cardiomyocytes and the extracellular matrix, and the administration of the active form of vitamin D can reduce or prevent this remodeling, by acting on anatomical, functional, molecular, and genetic aspects of cardiac hypertrophy and dysfunction that lead to heart failure with preserved ejection fraction (HFpEF)

  • Vitamin D represents a group of secosteroids involved in the calcium and phosphate metabolism; an adequate food intake and sunlight exposition are necessary to reach sufficient levels of vitamin D

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Summary

Introduction

Vitamin D is a group of secosteroids that physiologically improve the intestinal absorption of calcium and phosphate. Winter was the season when heart diseases were more frequent, possibly due to low levels of vitamin D. Calcitriol in turn directly suppresses the PTH gene transcription and the consequent hormone production, thereby increasing serum calcium levels. Several diseases can be associated with low vitamin D levels. It should be pointed out that the involvement of the vitamin D system in the pathogenesis of cardiovascular diseases is quite intricate. Within this context, a relevant role is played by the autocrine/paracrine pathways locally activated by vitamin D inside atherosclerotic plaques [11,12]. It has been shown that vitamin D receptor (VDR) expression in human carotid plaques correlates with a reduction in major adverse cardiovascular events (MACE) [12]

Vitamin D Signaling
Vitamin D and Renin–Angiotensin–Aldosterone System
Vitamin D and Endothelial Dysfunction
Vitamin D and Heart Failure
Vitamin D Supplementations and Cardiovascular Health
Potential Impact of Calcium and Phosphate on Cardiovascular Risk
Findings
Conclusions
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