Downregulation of Pin1 in human atherosclerosis and its association with vascular smooth muscle cell senescence

We found that decreased Pin1 protein level in human atherosclerotic tissues and vascular smooth muscle cells (VSMCs) was related to increased VSMC senescence, and in vivo data from apolipoprotein E−/−mice showed that treatment of a Pin1 inhibitor led to accelerated atherosclerosis development. This research indicated that interventions targeted at Pin1, such as cell-specific drugs, are potential novel approaches to the retardation of atherosclerosis, in which VSMC senescence has a prominent role. Patients with atherosclerosis may benefit from pharmacologic interference with Pin1.