Vascular calcification is recently considered as one of the major complications and an independent risk factor of cardiovascular diseases. Although vascular calcification was commonly regarded as a passive process of mineral adsorption or precipitation, it tends to be an active process associated with the expression of growth factors, matrix proteins, and other bone-related proteins. There are 2 main types of vascular calcification. Intimal calcification is found in atherosclerotic plaques and is associated with the vascular events such as myocardial infarction. Medial calcification is usually associated with age and chronic kidney disease patients, which leads to increased vascular stiffness and reduced vascular compliance. Interestingly, our vascular calcification model using ApoE deficient mice showed intima calcification at sites of atherosclerotic plaques under high fat diet with ovariectomy. Thus, lipid metabolism is one of the therapeutic targets to prevent intima calcification of aorta. Previously we reported that ezetimibe significantly prevented atherosclerosis through lipid-lowering effects in ApoE-deficient mice. Based on these findings, we speculate that ezetimibe might prevent aortic intima calcification, which may give us the benefits to decrease vascular events.
Keywords: RANKL, vascular calcification, atherosclerosis, ezetimibe, Intimal calcification, sclerotic plaques, myocardial infarction, Medial calcification, ApoE deficient, aorta, Ectopic calcification, myocardial in-farction, aortic SMC, BMP-2, NFB (RANK), osteoprotegerin (OPG), preosteoclastic cells, dendritic cells, fibroblasts, Peyer's patches, osteoclast apoptosis, TNF, OPG, human aortic smooth muscle cell (HASMC), ovariec-tomy, 3-hydroxy-3-methylglutaryl co-enzyme A (HMG-CoA), Niemann-Pick C1 Like 1, LDL cholesterol (LDL-C), triglyceride
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