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Using a quantitative statistical approach, we created a 3D atlas of embryonic cardiac morphogenesis from a collection of mouse specimens. The atlas includes the average shape of tissue geometry over time and its range of variability, and it enabled us to identify the onset of cardiac left–right asymmetry.
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.
