Control of vascular smooth muscle cell growth by cyclin-dependent kinase inhibitory proteins and its implication in cardiovascular disease

While quiescence is a defining characteristic of differentiated vascular sm ooth muscle cells (VSMCs) residing within the medial layer of elastic arter ies in the adult organism, mature VSMCs can undergo phenotypic modulation a nd reenter the cell cycle in response to several physiological and patholog ical stimuli. Abnormal VSMC proliferation is thought to contribute to the p athogenesis of vascular occlusive lesions, including atherosclerosis, vesse l renarrowing after successful angioplasty (restenosis), and graft atherosc lerosis after coronary transplantation. Therefore, elucidating the molecula r mechanisms limiting VSMC growth is currently the subject of active resear ch. This review will focus on the role of cyclin-dependent kinase inhibitor y proteins in the regulation of VSMC proliferation and its implication in i ntimal lesion formation during the pathogenesis of vascular proliferative d iseases.