Coronary artery disease and atherothrombosis are complex pathologic entities leading to poor clinical outcome and high cardiac mortality. Coronary artery revascularization strategies, such as percutaneous coronary intervention (PCI) in an effort to restore myocardial blood reperfusion, may only partially treat ischemic heart disease. PCI has revolutionized the revascularization for ischemiarelated cardiovascular diseases such as stable angina and acute coronary syndrome. Post-PCI restenosis, however, remains a major problem to overcome. Following the mechanical stretch, restenosis takes place in concert with the proliferation and migration of smooth muscle cells (SMCs) from the tunica media through the disruption of intima or endothelial barrier, and eventually leads to narrowed vascular lumen and obstruction. As the central pathogenetic event of restenosis, vascular neointimal hyperplasia occurs gradually as a result of the imbalance between SMC death and proliferation. Despite ample efforts, the precise mechanisms underscoring transition from initial apoptosis of vascular SMCs to apoptosis resistant proliferation remains unclear. As a conservative regulatory avenue found in nearly all mammalian cell types, autophagy plays a unique role in the delicate control on cell fate in the development of neointimal hyperplasia in post-PCI restenosis. In this mini-review, we will focus on how apoptosis, autophagy, and the cross-talk between the two govern cell death or proliferation in restenosis pathogenesis, particularly in neointimal hyperplasia involving SMCs.
Keywords: Apoptosis, autophagy, percutaneous coronary intervention, restenosis, neointimal hyperplasia, vascular smooth muscle cell.