5. Genomic and nongenomic controls of vitamin D on cardiovascular health and disease
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Ectopic or vascular calcification caused primarily by dysregulation of vitamin D and phosphate homeostasis is a major contributor to development of atherosclerosis and cardiovascular disease (CVD). Both deficiencies and excesses of vitamin D affect cardiovascular factors that mediate development of CVD. Atherosclerosis results from accumulation of plaque which is comprised of oxidized lipids, cellular debris, fibrin material and marked calcification. Vitamin D deficiency affects macrophage activation, adhesion and migration, which underlies the ‘response to injury’ hypothesis that initiates atherosclerotic progression. Vitamin D coupled with other epigenetic modifications can subdue cellular inflammation, reduce age-related systolic hypertension and vascular rigidity, and improve overall endothelial functions. Thus, understanding molecular changes and pathways that preserve function and integrity of vascular endothelia and smooth muscle cells will enable investigators to development effective dietary and/or therapeutic measures to remediate CVD. This chapter will explore the major contributions of vitamin D in controlling vascular endothelial and smooth muscle cell integrity, activation and inflammation. Emphasis is placed on: (1) evidence that links vitamin D deficiency to cardiovascular disease; (2) redox sensitivity and control of the vitamin D receptor; (3) role of vitamin D in augmenting the antioxidant network associated with the transcription factor, nuclear factor (erythroid-derived 2)-like 2; and (4) the association of vitamin D with fibroblast growth factor 23 and Klotho, the endocrine axis which regulates phosphate homeostasis among bone, parathyroid gland, and kidney.