This review summarizes the pathological role of HIF-1 in promoting atherosclerosis progression through foam cell formation, endothelial dysfunction, and inflammation.
May guide HIF-1 inhibitor development; leaves open clinical efficacy in atherosclerosis.
Atherosclerosis is by far the most frequent underlying cause of coronary artery disease, carotid artery disease and peripheral arterial disease, and is associated with high morbidity and mortality. Hypoxic areas are known to be present in human atherosclerotic lesions, and lesion progression is associated with the formation of lipid-loaded macrophages, increased local inflammation and angiogenesis. The key regulator of hypoxia, hypoxia-inducible factor 1 (HIF-1), plays a key role in the progression of atherosclerosis by initiating and promoting the formation of foam cells, endothelial cell dysfunction, apoptosis, increasing inflammation and angiogenesis. The objective of this review is to summarise the pathological role of HIF-1 in the progression of atherosclerosis.
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Gao et al. (2012) studied this question.
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