Premature cell senescence promotes vascular smooth muscle cell phenotypic modulation and resistance to re-differentiation

DNA damage and senescence induce genes associated with de-differentiated/fibromyocytic VSMCs, and persistence of these cells in vivo. Failure of senescent VSMCs to re-express contractile markers during re-differentiation suggests that VSMC senescence may promote atherosclerosis and neointima formation in part by inhibiting their re-differentiation.