“…However, VSMCs undergo phenotypic switching after arterial injury, becoming osteochondrocyte-like cells, foam cells, or myofibroblasts [ 8 , 9 ]. This process includes a decrease in the expression of genes related to VSMC differentiation and an increase in VSMC migration, proliferation, and the production of extracellular matrix (ECM) elements necessary for vascular repair [ 10 , 11 ], which is critical for the formation of arterial lesions and vascular remodeling [ 6 ]. Phenotypically modified VSMCs contribute to various cardiovascular diseases such as atherosclerosis, aortic aneurysm, transplant vasculopathy, intimal hyperplasia and restenosis, vascular calcification, hypertension, and aberrant tumor vasculature [ 12 , 13 , 14 , 15 ].…”