Abstract
The aim of the present paper was to review the most important mechanisms explaining the possible association of vitamin D deficiency and cardiovascular diseases, focusing on recent experimental and clinical data. Low vitamin D levels favor atherosclerosis enabling vascular inflammation, endothelial dysfunction, formation of foam cells, and proliferation of smooth muscle cells. The antihypertensive properties of vitamin D include suppression of the renin-angiotensin-aldosterone system, renoprotective effects, direct effects on endothelial cells and calcium metabolism, inhibition of growth of vascular smooth muscle cells, prevention of secondary hyperparathyroidism, and beneficial effects on cardiovascular risk factors. Vitamin D is also involved in glycemic control, lipid metabolism, insulin secretion, and sensitivity, explaining the association between vitamin D deficiency and metabolic syndrome. Vitamin D deficit was associated in some studies with the number of affected coronary arteries, postinfarction complications, inflammatory cytokines and cardiac remodeling in patients with myocardial infarction, direct electromechanical effects and inflammation in atrial fibrillation, and neuroprotective effects in stroke. In peripheral arterial disease, vitamin D status was related to the decline of the functional performance, severity, atherosclerosis and inflammatory markers, arterial stiffness, vascular calcifications, and arterial aging. Vitamin D supplementation should further consider additional factors, such as phosphates, parathormone, renin, and fibroblast growth factor 23 levels.
Highlights
Vitamin D exists in two forms: D2 and D3
Vitamin D receptors were found in other tissues, as well, including the brain, cardiomyocytes, vascular smooth muscle cells, endothelial cells, pancreatic beta-cells, skeletal muscle, breast, prostate, colon, macrophages, and skin, exerting several pleiotropic effects, and their expression decreases with age
Observational data support the link between vitamin D status and cardiovascular diseases, and vitamin D deficiency can be considered a cardiovascular risk marker
Summary
Vitamin D exists in two forms: D2 (ergocalciferol) and D3 (cholecalciferol). Vitamin D3, “the sunshine vitamin,” is synthetized in the human epidermis via ultraviolet irradiation, or it may be consumed in the form of oily fish or supplements. Calcitriol, the active form of vitamin D, binds to vitamin D receptors in the intestines, bones, and kidneys to increase calcium absorption from the intestines, promote calcium deposition in bones, and decrease parathyroid hormone concentrations (PTH). Vitamin D receptors were found in other tissues, as well, including the brain, cardiomyocytes, vascular smooth muscle cells, endothelial cells, pancreatic beta-cells, skeletal muscle, breast, prostate, colon, macrophages, and skin, exerting several pleiotropic effects, and their expression decreases with age. Existing data from laboratory studies, epidemiologic and experimental research and prevention trials, suggest that vitamin D reduces the risk of cardiovascular disease, and a large, randomized, primary prevention trial, with adequate dosing, combining cholecalciferol and omega-3 fatty acids, is ongoing: the VITAL study. The aim of the present paper was to review the most important mechanisms explaining the possible association of vitamin D deficiency and cardiovascular diseases, focusing on recent experimental and clinical data
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