骨骼肌缺血–再灌注损伤的病理机制与研究进展综述
A Review of Pathological Mechanisms and Research Progress of Skeletal Muscle Ischemia-Reperfusion Injury
DOI: 10.12677/acm.2025.1582375, PDF,    科研立项经费支持
作者: 徐竟菲*：福建中医药大学骨伤学院，福建 福州；李彦丰#：河南省洛阳正骨医院(河南省骨科医院)手外显微一科，河南 洛阳
关键词: 缺血–再灌注损伤；骨骼肌；病理机制；研究进展；Ischemia-Reperfusion Injury； Skeletal Muscle； Pathological Mechanism； Research Progress
摘要: 骨骼肌缺血–再灌注损伤(Ischemia-Reperfusion Injury, IRI)广泛发生于外伤、血管重建手术、肢体再植及挤压综合征等临床场景，其病理过程涉及能量代谢障碍、氧化应激、钙超载、炎症激活与程序性细胞死亡等多个环节。近年来研究发现，这些机制之间存在密切交叉调控，如cFLIP、caspase-8、RIPK1/RIPK3等分子桥梁在不同死亡方式之间的转换中发挥关键作用。同时，补体系统、代谢重编程、自噬与免疫网络共同构成IRI的病理网络。本文系统梳理近年研究进展，提出信号交叉、代谢调控与个体化干预的未来研究方向，旨在为深入理解IRI的复杂机制及开发多靶点干预策略提供理论依据与研究思路。
Abstract: Skeletal muscle Ischemia-Reperfusion Injury (IRI) occurs extensively in clinical scenarios such as trauma, vascular reconstruction surgery, limb replantation, and crush syndrome. Its pathological process involves multiple links, including energy metabolism dysfunction, oxidative stress, calcium overload, inflammatory activation, and programmed cell death. Recent studies have found that there is close cross-regulation among these mechanisms. For example, molecular bridges such as cFLIP, caspase-8, and RIPK1/RIPK3 play a key role in the transition between different death modalities. Meanwhile, the complement system, metabolic reprogramming, autophagy, and immune network together constitute the pathological network of IRI. This article systematically reviews recent research progress and proposes future research directions in signal crosstalk, metabolic regulation, and individualized intervention, aiming to provide a theoretical basis and research ideas for in-depth understanding of the complex mechanisms of IRI and the development of multi-target intervention strategies.
文章引用：徐竟菲, 李彦丰. 骨骼肌缺血–再灌注损伤的病理机制与研究进展综述[J]. 临床医学进展, 2025, 15(8): 1365-1372. https://doi.org/10.12677/acm.2025.1582375

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