Vascular smooth muscle cell in atherosclerosis

Abstract Vascular smooth muscle cells ( VSMC s) exhibit phenotypic and functional plasticity in order to respond to vascular injury. In case of the vessel damage, VSMC s are able to switch from the quiescent ‘contractile’ phenotype to the ‘proinflammatory’ phenotype. This change is accompanied by decrease in expression of smooth muscle ( SM )‐specific markers responsible for SM contraction and production of proinflammatory mediators that modulate induction of proliferation and chemotaxis. Indeed, activated VSMC s could efficiently proliferate and migrate contributing to the vascular wall repair. However, in chronic inflammation that occurs in atherosclerosis, arterial VSMC s become aberrantly regulated and this leads to increased VSMC dedifferentiation and extracellular matrix formation in plaque areas. Proatherosclerotic switch in VSMC phenotype is a complex and multistep mechanism that may be induced by a variety of proinflammatory stimuli and hemodynamic alterations. Disturbances in hemodynamic forces could initiate the proinflammatory switch in VSMC phenotype even in pre‐clinical stages of atherosclerosis. Proinflammatory signals play a crucial role in further dedifferentiation of VSMC s in affected vessels and propagation of pathological vascular remodelling.