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- W2008227377 abstract "Vitamin D<sub>3</sub> deficiency is a highly prevalent condition worldwide. Clinically, vitamin D<sub>3</sub> has a key role in calcium homeostasis and bone mineralization and has recently been implicated in the pathogenesis and/or progression of several acute and chronic illnesses, including cardiovascular disease (CVD). Accumulating evidence from observational, prospective studies suggests that low levels of serum 25-hydroxyvitamin D<sub>3</sub> are independently associated with an increased risk of CVD events and death. The molecular mechanisms of this association remain incompletely understood. A variety of biologically plausible mechanisms may mediate a cardiovascular role for the active metabolite of vitamin D<sub>3</sub>. 1-α,25-dihydroxyvitamin D<sub>3</sub> regulates the renin–angiotensin system, suppresses proliferation of vascular cell smooth muscle, improves insulin resistance and endothelial cell-dependent vasodilation, inhibits myocardial cell hypertrophy, exerts anticoagulant and antifibrotic activity, and modulates macrophage activity and cytokine generation. Overall, the high prevalence of vitamin D<sub>3</sub> deficiency and the plausible biological mechanisms linking this to CVD risk suggest that the treatment of vitamin D<sub>3</sub> deficiency to prevent CVD is a promising field to explore. Large placebo-controlled randomized clinical trials are urgently needed to determine whether vitamin D supplementation could have any potential benefit in reducing future CVD events and mortality risk." @default.
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- W2008227377 date "2012-02-01" @default.
- W2008227377 modified "2023-10-10" @default.
- W2008227377 title "Vitamin D, Thrombosis, and Hemostasis: More than Skin Deep" @default.
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- W2008227377 doi "https://doi.org/10.1055/s-0031-1300957" @default.
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