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In mouse models of atherosclerosis, smooth muscle cell (SMC)-specific disruption of a gene associated with coronary artery disease in human genome-wide association studies alters atherosclerotic plaque features by promoting SMC transition to an atherogenic phenotype.
Global or macrophage-specific knockout of Trpm2, which encodes the calcium-permeable ion channel TRPM2, protects mice against atherosclerosis induced by a high-fat diet. Mechanistically, activation of TRPM2 and the scavenger receptor CD36 promote the transformation of macrophages into inflammatory foam cells, thereby accelerating the development and progression of atherosclerosis.
