Title:Life and Death Partners in Post-PCI Restenosis: Apoptosis, Autophagy, and The Cross-talk Between Them
Volume: 19
Issue: 9
关键词:
细胞凋亡，自噬，经皮冠状动脉介入治疗，再狭窄，新生内膜增生，血管平滑肌细胞
摘要: 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.
