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线粒体跨细胞转移在脑缺血/再灌注损伤中的作用机制

安瑞舒^1,2,3, 秦文秀^1,2,3, 杨建^1,2, 许军峰^1,2,*

¹天津中医药大学第一附属医院针灸科，天津 301617；²国家中医针灸临床医学研究中心，天津 301617；³天津中医药大学，天津 301617

摘要

缺血性脑卒中(ischemic stroke, IS)是指脑血管阻塞引起的脑组织血液循环障碍和神经功能缺损的急性脑血管疾病，是全球最常见的死亡原因之一。静脉溶栓和血管内血栓切除术等疗法可通过再灌注打开闭塞的脑血管，恢复血流，但缺血/再灌注(ischemia/reperfusion, I/R)可能引发氧化应激、电解质紊乱、炎性反应等病理变化，导致脑水肿和颅内出血等继发性组织损伤。因此，减轻脑缺血/再灌注损伤(cerebral ischemia-reperfusion injury, CIRI)至关重要。线粒体作为细胞器通常存在于细胞内部，但在CIRI的刺激下，线粒体及其组分可通过隧道纳米管(tunneling nanotubes, TNTs)、缝隙连接(gap junctions, GJs)、释放和捕获细胞外囊泡(extracellular vesicles, EVs)等方式跨细胞转移，影响脑部组织细胞。针对CIRI的线粒体跨细胞转移疗法可减轻氧化应激损伤、改善神经元能量代谢、调节神经炎症、促进神经修复和再生，被视为一种具有潜力的治疗方法，因此深入探究线粒体跨细胞转移的作用机制有望为CIRI的治疗开辟全新临床途径。本文深入探究了线粒体跨细胞转移的分子机制及其在CIRI治疗中的效果，有望拓宽临床治疗思路，为CIRI的治疗提供新方向。

关键词： 线粒体跨细胞转移; 脑缺血/再灌注损伤; 缺血性脑卒中; 隧道纳米管; 缝隙连接

Mechanism of mitochondrial transcellular transfer in cerebral ischemia-reperfusion injury

AN Rui-Shu^1,2,3, QIN Wen-Xiu^1,2,3, YANG Jian^1,2, XU Jun-Feng^1,2,*

¹Department of Acupuncture, First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China；²National Clinical Research Center for Chinese Medicine Acupuncture and Moxibustion, Tianjin 301617, China；³Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China

Abstract

Ischemic stroke (IS) is an acute cerebrovascular disease in which blood circulation to brain tissue and neurological function are impaired due to obstruction of cerebral blood vessels, and it is one of the most common causes of death worldwide. Therapies such as intravenous thrombolysis and endovascular thrombectomy can open occluded cerebral vessels and restore blood flow through reperfusion, but ischemia/reperfusion (I/R) may trigger pathological processes such as oxidative stress, electrolyte disorders, and inflammatory responses, leading to secondary tissue damage such as cerebral edema and intracranial hemorrhage. Therefore, it is crucial to mitigate cerebral ischemia-reperfusion injury (CIRI). Mitochondria, as organelles, usually exist inside cells. However, under the stimulation of CIRI, mitochondria and their components can affect brain tissue cells by transcellular transfer through tunneling nanotubes (TNTs), gap junctions (GJs), and releasing and capturing of extracellular vesicles (EVs), etc. The mitochondrial transcellular transfer therapy for CIRI can reduce oxidative stress damage, improve neuronal energy metabolism, regulate neuroinflammation, and promote neural repair and regeneration. Mitochondrial transcellular transfer is regarded as a promising therapeutic approach for the treatment of CIRI, and in-depth investigation of the mechanism of mitochondrial transcellular transfer is expected to open up a new clinical pathway for the treatment of CIRI. This paper explores the molecular mechanism of mitochondrial transcellular transfer and its effects in the treatment of CIRI, which is expected to broaden clinical therapeutic approaches and provide a new direction for the treatment of CIRI.

Key words: mitochondrial transcellular transfer; cerebral ischemia-reperfusion injury; ischemic stroke; tunneling nanotube; gap junction

收稿日期：　　录用日期：

通讯作者：许军峰　　E-mail:

DOI: 10.13294/j.aps.2026.0030

引用本文：

安瑞舒, 秦文秀, 杨建, 许军峰. 线粒体跨细胞转移在脑缺血/再灌注损伤中的作用机制[J]. 生理学报 2026; 78 (2): 295-305.

AN Rui-Shu, QIN Wen-Xiu, YANG Jian, XU Jun-Feng. Mechanism of mitochondrial transcellular transfer in cerebral ischemia-reperfusion injury. Acta Physiol Sin 2026; 78 (2): 295-305 (in Chinese with English abstract).