ArticleFrontiers in physiology2026
Genetic ablation of TRPC6 facilitated age-dependent atherosclerosis progression in an ApoE-/- mouse model.
Article in Frontiers in physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: TRPC6 channels are expressed in endothelial cells, smooth muscle cells, and macrophages within the atherosclerotic segments of conduit blood vessels. Genetic or pharmacological inactivation of TRPC6 was variably associated with the development of atherosclerosis, a risk factor for myocardial infarction, ischemic stroke, and/or peripheral vascular disease. Methods: We used two genetically matched mouse strains, ApoE Results: We assessed atherosclerotic lesion progression in mouse aortas by measuring their area, fibrous cap thickness, and calcification. We found that one-year-old mature mice had similar aortic atherosclerosis. However, aged 1.5-year-old ApoE Conclusions: Age-dependent, spontaneous atherosclerosis progression was greater in aged but not mature ApoE
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