Closing the Cycle

Abstract

See related article, pages 1141–1150 Smooth muscle cell (SMC) accumulation in the arterial intima is a key event in restenosis after angioplasty and bypass surgery and in the development of atherosclerotic lesions.1 Restenosis, which is defined as “the arterial healing response after injury incurred during transluminal coronary revascularization,” has been the principal drawback of percutaneous coronary interventions (PCI) since their introduction. The accumulation of arterial SMCs is caused by a combination of proliferation and directed migration of arterial SMCs from the media into the intima. Both these activities can be induced by cytokines and growth factors produced within the arterial wall and circulating cells in response to the vascular injury. A commonly accepted model of the response to arterial injury suggests that growth factors are released after injury, thereby changing the composition of the extracellular matrix and triggering a proliferation and migration program. SMCs undergo a phenotypic modulation from a contractile to a synthetic phenotype (dedifferentiation), proliferate into the media, migrate from the media into the intima, and subsequently form the neointima. SMC transition from G1 to Gs cell …