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作 者:陈浩楠 王嵛 CHEN Haonan;WANG Yu(College of Physical Education,Henan University,Kaifeng 475001,CHN;Fuwai Huazhong Hospital for Cardiovascular Diseases,Key Laboratory of Coronary Heart Disease,Zhengzhou 451450,CHN)
机构地区:[1]河南大学体育学院,河南开封475001 [2]阜外华中心血管病医院冠心病重点实验室,河南郑州451450
出 处:《河南大学学报(医学版)》2025年第1期1-11,共11页Journal of Henan University:Medical Science
基 金:河南省自然科学基金(242300421516)。
摘 要:心肌缺血再灌注损伤(MIRI)是由于缺血心肌快速再通导致的心肌损伤加重。近年来,研究MIRI的病理生理机制、确定有效的靶点和药物倍受关注。细胞焦亡作为一种炎症性程序性死亡方式正被重视,它与氧化应激、钙超载、坏死性凋亡及细胞凋亡等机制共同参与MIRI的发生并影响其发展。本文探讨了细胞焦亡在MIRI中的机制及其与其他机制的关系,重点介绍了非心肌细胞如何调节心肌细胞焦亡,并参与MIRI的进程。新型小分子药物和中药在调控细胞焦亡方面的研究进展,对缓解MIRI具有重要作用。尽管已有许多保护药物,但临床应用仍不足,因此需要进一步探索和验证,以扩大其应用。未来研究需解决靶向调控细胞焦亡以早期抑制MIRI的关键问题。Myocardial ischemia-reperfusion injury(MIRI)is an exacerbation of myocardial damage due to rapid recanalization of ischemic myocardium.In recent years,research on the pathophysiological mechanisms of MIRI and identification of effective targets and drugs have attracted much attention.Cellular pyroptosis is being emphasized as a mode of inflammatory programmed death,which is involved in the development of MIRI in conjunction with oxidative stress,calcium overload,necrotic apoptosis,and apoptosis,among other mechanisms,to influence its progression.This article discusses the mechanism of cellular focalization in MIRI and its relationship with other mechanisms,focusing on how non-cardiomyocytes regulate cardiomyocyte focalization and participate in the process of MIRI.The research progress of novel small molecule drugs and traditional Chinese medicine in regulating cellular focal death has an important role in alleviating MIRI.Despite the availability of many protective drugs,clinical applications are still insufficient and thus need to be further explored and validated to expand their applications.Future studies need to address the critical issue of targeting and regulating cellular focal death for early inhibition of MIRI.
分 类 号:R542.2[医药卫生—心血管疾病]
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