Vitamin D as A Protector of Arterial Health: Potential Role in Peripheral Arterial Disease Formation

被引:33
作者
Krishna, Smriti Murali [1 ]
机构
[1] James Cook Univ, Coll Med & Dent, Townsville, Qld 4811, Australia
关键词
vitamin D; 25(OH)D; peripheral arterial disease; peripheral arterial occlusive disease; abdominal aortic aneurysm; epigenetics; ABDOMINAL AORTIC-ANEURYSM; SERUM 25-HYDROXYVITAMIN D; ENDOPLASMIC-RETICULUM STRESS; BREAST-CANCER CELLS; D-RECEPTOR; D DEFICIENCY; 1,25-DIHYDROXYVITAMIN D-3; GENOME-WIDE; ENDOTHELIAL-CELLS; CARDIOVASCULAR-DISEASE;
D O I
10.3390/ijms20194907
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Atherosclerotic occlusive diseases and aneurysms that affect large and medium-sized arteries outside the cardiac and cerebral circulation are collectively known as peripheral arterial disease (PAD). With a rise in the rate of aging population worldwide, the number of people diagnosed with PAD is rapidly increasing. The micronutrient vitamin D is an important steroid hormone that acts on many crucial cellular mechanisms. Experimental studies suggest that optimal levels of vitamin D have beneficial effects on the heart and blood vessels; however, high vitamin D concentrations have been implicated in promoting vascular calcification and arterial stiffness. Observations from various clinical studies shows that deficiency of vitamin D has been associated with a greater risk of PAD. Epidemiological studies have often reported an inverse relation between circulating vitamin D status measured in terms of 25-hydroxivitamin D [25(OH)D] levels and increased cardiovascular disease risk; however, randomized controlled trials did not show a consistent positive effect of vitamin D supplementation on cardiovascular disease risk or events. Even though PAD shares all the major risk factors with cardiovascular diseases, the effect of vitamin D deficiency in PAD is not clear. Current evidence suggests a strong role of vitamin D in promoting genomic and epigenomic changes. This review summarises the current literature that supports the notion that vitamin D deficiency may promote PAD formation. A better understanding of underlying pathological mechanisms will open up new therapeutic possibilities which is the main unmet need in PAD management. Furthermore, epigenetic evidence shows that a more holistic approach towards PAD prevention that incorporates a healthy lifestyle, adequate exercise and optimal nutrition may be more effective in protecting the genome and maintaining a healthy vasculature.
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