Chang Chen, Huang Wan-Zhong, Cai Ru-Ping, Mo Li-Rong, Wu Qiang, Su Qiang
Department of Cardiology, The First Affiliated Hospital of Xi'an Medical University, Xi'an 710077, Shanxi, People's Republic of China.
Department of Cardiology, Jiangbin Hospital of Guangxi Zhuang Autonomous Region, Nanning 530021, Guangxi, People's Republic of China.
Int J Med Sci. 2025 Jan 1;22(1):132-139. doi: 10.7150/ijms.105295. eCollection 2025.
Coronary microembolization (CME) is defined as atherosclerotic plaque erosion, spontaneous rupture, or rupture of the plaque while undergoing interventional therapy resulting in the formation of tiny emboli that obstruct the coronary microcirculatory system. For percutaneous coronary intervention, CME is a major complication, with a periprocedural incidence of up to 25%. Recent studies have demonstrated that regulatory cell death (RCD) exerts a profound influence on CME through its modulation of inflammatory responses, oxidative stress, cell death, and angiogenesis. RCD, including apoptosis, autophagy, and pyroptosis, is a unique class of genetically highly regulated death patterns pervasive in instances of coronary microembolization. The aim of this review is to summarize the currently known molecular mechanisms underlying CME. Further investigations of the RCD mechanisms may unravel new avenues for the prevention and treatment of CME.
冠状动脉微栓塞（CME）的定义是动脉粥样硬化斑块侵蚀、自发破裂，或在介入治疗过程中斑块破裂，导致形成微小栓子，阻塞冠状动脉微循环系统。对于经皮冠状动脉介入治疗，CME是一种主要并发症，围手术期发生率高达25%。最近的研究表明，调节性细胞死亡（RCD）通过调节炎症反应、氧化应激、细胞死亡和血管生成，对CME产生深远影响。RCD包括细胞凋亡、自噬和焦亡，是一类独特的、在冠状动脉微栓塞情况下普遍存在的、基因高度调控的死亡模式。本综述的目的是总结目前已知的CME潜在分子机制。对RCD机制的进一步研究可能为CME的预防和治疗开辟新途径。
