主管单位:中华人民共和国
国家卫生健康委员会
总编辑:杨秋
编辑部主任:吴翔宇
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单位:首都医科大学附属北京安贞医院整形美容激光中心,北京100029
英文单位:Plastic Surgery and Laser Center Beijing Anzhen Hospital Capital Medical University Beijing 100029 China
英文关键词:Ischemia-reperfusioninjury;Programmedcelldeath;Molecularmechanism;Interventionmeasures
缺血再灌注损伤(IRI)是急性心肌梗死、脑卒中及器官移植等重大疾病临床治疗中的关键瓶颈问题。传统理论认为IRI主要由氧化应激介导,属于一种被动型组织损伤过程;然而,随着分子生物学技术的进步,程序性细胞死亡(PCD)的多样性与复杂性逐渐被揭示。目前研究证实,细胞在IRI中并非仅通过单一途径发生死亡,而是涉及凋亡、坏死性凋亡、焦亡、铁死亡、自噬、泛凋亡、铜死亡及双硫死亡等多种死亡模式共同参与调控的病理进程。本文系统综述了上述PCD方式在IRI中的核心分子机制及潜在的靶向干预策略,旨在深入解析IRI的病理本质,为优化临床防治方案、改善患者预后提供理论依据。
Ischemia-reperfusion injury (IRI) is a key bottleneck in the clinical treatment of major diseases such as acute myocardial infarction, stroke and organ transplantation. Traditional theories hold that IRI is mainly mediated by oxidative stress and is a passive process of tissue damage. However, with the advancement of molecular biological techniques, the diversity and complexity of programmed cell death (PCD) have been gradually revealed. Current studies have confirmed that cell death during IRI is not mediated through a single pathway,but rather involves a pathological process regulated by multiple modes of cell death,including apoptosis, necroptosis, pyroptosis, ferroptosis, autophagy, panoptosis, cuproptosisand disulfidptosis. This paper systematically reviews the core molecular mechanisms and potential targeted intervention strategies of the above PCD modes in IRI, aiming to deeply analyze the pathological essence of IRI and provide a theoretical basis for optimizing clinical prevention and treatment plans and improving patient prognosis.
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