Abstract
Changes in vascular smooth muscle cells (vSMC) have proven to be a contributing factor to the development and progression of atherosclerosis. Following arterial injury, vSMCs can undergo differentiation to acquire phenotypes resembling foam cells, mesenchymal stem cells, and osteochondrogenic cells, which can all aid in intimal plaque formation and promote vascular stenosis. Dynamin-related protein 1 (Drp1) is a cytosolic GTPase that mediates mitochondrial fission. Increased mitochondrial fission is affiliated with SMC proliferation and migration, thus increasing the formation of neointimal hyperplasia, forming an anatomical basis for atherosclerosis development.
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