A Review on Vitamin D Deficiency and Risk of Cardiovascular Disease View PDF

Calcium and phosphate are physiologically absorbed more efficiently by the intestinal tract due to vitamin D. Cholecalciferol (vitamin D3) and ergocalciferol (vitamin D2) are the most important components of vitamin D. Among people suffering from CVD, there was a seasonality associated with vitamin D. It has been shown that heart disease is more common during winter, possibly because vitamin D levels are low. With food, you can take cholecalciferol and ergocalciferol. There are two distinct metabolic processes that occur after vitamin D2 is consumed through food. As a result of liver metabolism, vitamin D2 becomes 25-hydroxyvitamin D (25(OH)D), which is converted in the kidney to 1,25(OH)2 D (calcitriol) by CYP27B1. Several feedback mechanisms regulate calcitriol production in the endocrine system. A reduction in calcium plasma levels results in the release of parathyroid hormone (PTH), which stimulates calcium calcitriol production. As a result, calcium increases serum calcium levels by directly suppressing PTH gene transcription and subsequent hormone production. Moreover, calcium-sensing receptor gene transcription and protein expression are also upregulated by calcitriol. In addition, vitamin D inhibits CYP27B1 from regulating its own production. Furthermore, cholecalciferol is synthesized by the skin under sunlight exposure. Several factors affect how much sunlight is required to satisfy our vitamin D requirements, including skin pigmentation, age, latitude, season of the year, or time of day. Vitamin D deficiency can contribute to several diseases. Vitamin D deficiency has long been associated with rickets. Moreover, low vitamin D levels can contribute to chronic diseases such as atherosclerosis, heart disease, high blood pressure, heart failure, type 2 diabetes, cancer, and immunological conditions. The results of randomized clinical trials (RCTs) designed to prove vitamin D supplementation’s therapeutic effects have been inconclusive despite the pathogenic link between vitamin D deficiency and these diseases. Although the role of vitamin D in CVD pathogenesis is quite complex, it should be noted. Furthermore, vitamin D locally activates autocrine/paracrine pathways in atherosclerotic plaques, which play a supportive role within this context. Human carotid plaques expressing VDRs were associated with less major adverse cardiovascular events (MACEs). 

VDR, a cytosolic receptor protein that activates transcription of targeted genes in response to ligand binding, mediates vitamin D’s biological effects. The VDR gene is located on chromosome 12q and belongs to the nuclear receptor transcription factor family. Vitamin D and retinoid X receptors bind to the VDR, activating it. This results in the activated heterodimeric receptor complex translocating into the nucleus where it engages specific nucleotide sequences called vitamin D response elements (VDREs). Within hours or days, the latter regulate vitamin D-sensitive gene transcription. The VDR is also localized at the level of cell membrane, so vitamin D can also affect gene expression quickly through this classical signaling pathway [3]. Histone modification and other epigenetic mechanisms are likely to trigger these rapid effects. There have been many studies, but the tissue distribution of VDR has not yet been clearly defined. The receptor is certainly expressed in cells of the skeleton, bowel, heart, and endothelium. There are several studies showing the presence of CYP27B1, which allows us to gain a better understanding of how vitamin D affects endothelial and cardiomyocyte functions locally. Atherosclerotic plaques may develop as a result of local deficiency of vitamin D in tissues [4].