摘要
冠状动脉疾病和动脉粥样硬化血栓形成是复杂的病理实体,导致不良的临床结果和高心脏病死亡率。冠状动脉血运重建策略,例如经皮冠状动脉介入治疗(PCI)以恢复心肌血液再灌注,可能仅部分治疗缺血性心脏病。 PCI已经彻底改变了缺血性心血管疾病(如稳定型心绞痛和急性冠状动脉综合征)的血运重建。然而,PCI后再狭窄仍然是需要克服的主要问题。在机械拉伸之后,再狭窄与来自中膜的平滑肌细胞(SMC)的增殖和迁移通过内膜或内皮屏障的破坏一起发生,并最终导致血管腔变窄和阻塞。作为再狭窄的中枢致病事件,由于SMC死亡和增殖之间的不平衡,血管新内膜增生逐渐发生。尽管做了大量努力,但强调从血管SMC的初始凋亡向细胞凋亡抗性增殖转变的确切机制仍不清楚。作为在几乎所有哺乳动物细胞类型中发现的保守调节途径,自噬在PCI后再狭窄中新内膜增生的发展中对细胞命运的精细控制中起独特作用。在这篇小型综述中,我们将关注细胞凋亡,自噬以及两者之间的交叉对话如何控制再狭窄发病机制中的细胞死亡或增殖,尤其是涉及SMC的新内膜增生。
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
图形摘要
Current Drug Targets
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.
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Cite this article as:
Life and Death Partners in Post-PCI Restenosis: Apoptosis, Autophagy, and The Cross-talk Between Them, Current Drug Targets 2018; 19 (9) . https://dx.doi.org/10.2174/1389450117666160625072521
DOI https://dx.doi.org/10.2174/1389450117666160625072521 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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