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• W2955297526 endingPage "657" @default.
• W2955297526 startingPage "646" @default.
• W2955297526 abstract "Although hyperlipidemia is established as a risk factor for vascular calcification, lipid-lowering drugs (statins) are clinically associated with progression of coronary calcification. At the cellular and molecular level, endothelial–mesenchymal transformation, microRNA, lncRNA, and autotaxin have been implicated in CVVD. At the clinical level, intense exercise and elite athleticism have been implicated, paradoxically, with increased coronary calcification. Calcific vascular and valvular disease (CVVD) is widespread and has major health consequences. Although coronary artery calcification has long been associated with hyperlipidemia and increased mortality, recent evidence suggests that its progression is increased in association with cholesterol-lowering HMG-CoA reductase inhibitors (‘statins’) and long-term, high-intensity exercise. A nationwide trial showed no cardiovascular benefit of vitamin D supplements. Controversy remains as to whether calcium deposits in plaque promote or prevent plaque rupture. CVVD appears to occur through mechanisms similar to those of intramembranous, endochondral, and osteophytic skeletal bone formation. New evidence implicates autotaxin, endothelial–mesenchymal transformation, and microRNA and long non-coding RNA (lncRNA) as novel regulatory factors. New therapeutic options are being developed. Calcific vascular and valvular disease (CVVD) is widespread and has major health consequences. Although coronary artery calcification has long been associated with hyperlipidemia and increased mortality, recent evidence suggests that its progression is increased in association with cholesterol-lowering HMG-CoA reductase inhibitors (‘statins’) and long-term, high-intensity exercise. A nationwide trial showed no cardiovascular benefit of vitamin D supplements. Controversy remains as to whether calcium deposits in plaque promote or prevent plaque rupture. CVVD appears to occur through mechanisms similar to those of intramembranous, endochondral, and osteophytic skeletal bone formation. New evidence implicates autotaxin, endothelial–mesenchymal transformation, and microRNA and long non-coding RNA (lncRNA) as novel regulatory factors. New therapeutic options are being developed. directional dependence with respect to physical properties such as stiffness and strength. An atherosclerotic plaque is anisotropic because it is composed of fibrous tissue, extracellular lipids, calcium deposits, and smooth muscle and inflammatory cells that are randomly aligned. a form of ectopic mineralization, in some cases evolving to form true bone and cartilage tissue in animal models and human. calcium buildup in the arteries that supply blood to the heart muscle; a reliable marker for assessing cardiovascular risk. mechanical or rupture at an interface. a numerical method for predicting the mechanical behavior of a material under given mechanical loads. It helps engineers to find areas of weakness and high stress. these modulate specific gene expression in a cell/tissue-selective manner. They are implicated in diverse roles, and their dysregulation leads to pathology and diseases. refers to a calcium deposit ≥50 μm in diameter. refers to a calcium deposit <50 μm in diameter. related multiple transmembrane proteins which function as high-affinity, sodium-dependent, phosphate transporters; they may also serve as phosphate sensors through heterodimerization induced by phosphate binding. receptor activator of nuclear factor κB ligand (also known as TNFSF11, OPGL, ODF) is secreted by osteoblastic cells. RANKL binds to RANK that is expressed on osteoclast precursors to induce osteoclastic differentiation and bone resorption; promotes vascular cell calcification in vitro. a model for atherosclerosis regression based on reversal of hyperlipidemia. This mouse model harbors several genetic modifications, including LDL receptor deficiency, apolipoprotein B-100 overexpression, and conditional deletion of microsomal triglyceride transfer protein. originally coined to describe a scattered distribution of calcium deposits that were found by intravascular ultrasound imaging (in distinction to larger coalescent deposits) to be a feature of vulnerable plaque. Given the resolution of intravascular ultrasound (IVUS), and the images shown in the reports, these deposits range in size, but they would be on the order of 1 mm in diameter. a parameter that determines whether a given material will rupture. When it reaches a critical value equal to or greater than the yield limit (tolerance) of the material, the material will rupture." @default.
• W2955297526 created "2019-07-12" @default.
• W2955297526 creator A5059995837 @default.
• W2955297526 creator A5062873812 @default.
• W2955297526 date "2019-09-01" @default.
• W2955297526 modified "2023-10-10" @default.
• W2955297526 title "Interactive and Multifactorial Mechanisms of Calcific Vascular and Valvular Disease" @default.
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