The Role of Mitochondria in Liver Ischemia-Reperfusion Injury: From Aspects of Mitochondrial Oxidative Stress, Mitochondrial Fission, Mitochondrial Membrane Permeable Transport Pore Formation, Mitophagy, and Mitochondria-Related Protective Measures.
The Role of Mitochondria in Liver Ischemia-Reperfusion Injury: From Aspects of Mitochondrial Oxidative Stress, Mitochondrial Fission, Mitochondrial Membrane Permeable Transport Pore Formation, Mitophagy, and Mitochondria-Related Protective Measures.
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线粒体在肝脏缺血再灌注损伤中的作用：从线粒体氧化应激、线粒体裂变、线粒体膜通透性运输孔形成、线粒体自噬以及线粒体相关保护措施等方面
DOI：
10.1155/2021/6670579
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发表时间：
2021
影响因子：
--
通讯作者：
Chen L
中科院分区：
文献类型：
--
作者：
Zhang H;Yan Q;Wang X;Chen X;Chen Y;Du J;Chen L
缺血再灌注损伤（IRI）确实是肝切除术、肝移植、外伤和低血容量性休克的主要并发症。大量研究证实微血管和实质损伤主要由活性氧（reactive oxygen species， ROS）引起，被认为是IRI的主要危险因素。在正常情况下，ROS作为细胞代谢的一种副产物，可以控制在正常水平。然而，当IRI发生时，线粒体氧化磷酸化被抑制。此外，氧化性呼吸链损伤导致大量消耗三磷酸腺苷（ATP）和大量ROS。此外，在IRI中，线粒体功能障碍涉及多个器官和组织。一方面，过多的自由基引起线粒体的损伤，如线粒体的结构、数量、功能、能量代谢等。另一方面，线粒体融合分裂障碍导致线粒体数量进一步减少，不足以清除过量的ROS，线粒体结构改变形成线粒体膜透性运输孔（mptp），导致细胞坏死和凋亡，器官衰竭，代谢功能障碍，增加发病率和死亡率。根据IRI的形成机制，已经发现或合成了多种针对特定靶点和细胞信号通路的物质来抑制或减缓肝脏IRI对机体的损伤。本文结合这一领域的研究进展，从线粒体氧化应激、线粒体融合与裂变、mPTP的形成以及相应的保护措施等方面阐述了线粒体在肝脏IRI中的作用。为今后的临床治疗和研究提供参考。
Ischemia-reperfusion injury (IRI) has indeed been shown as a main complication of hepatectomy, liver transplantation, trauma, and hypovolemic shock. A large number of studies have confirmed that microvascular and parenchymal damage is mainly caused by reactive oxygen species (ROS), which is considered to be a major risk factor for IRI. Under normal conditions, ROS as a kind of by-product of cellular metabolism can be controlled at normal levels. However, when IRI occurs, mitochondrial oxidative phosphorylation is inhibited. In addition, oxidative respiratory chain damage leads to massive consumption of adenosine triphosphate (ATP) and large amounts of ROS. Additionally, mitochondrial dysfunction is involved in various organs and tissues in IRI. On the one hand, excessive free radicals induce mitochondrial damage, for instance, mitochondrial structure, number, function, and energy metabolism. On the other hand, the disorder of mitochondrial fusion and fission results in further reduction of the number of mitochondria so that it is not enough to clear excessive ROS, and mitochondrial structure changes to form mitochondrial membrane permeable transport pores (mPTPs), which leads to cell necrosis and apoptosis, organ failure, and metabolic dysfunction, increasing morbidity and mortality. According to the formation mechanism of IRI, various substances have been discovered or synthesized for specific targets and cell signaling pathways to inhibit or slow the damage of liver IRI to the body. Here, based on the development of this field, this review describes the role of mitochondria in liver IRI, from aspects of mitochondrial oxidative stress, mitochondrial fusion and fission, mPTP formation, and corresponding protective measures. Therefore, it may provide references for future clinical treatment and research.
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影响因子：
--
作者：
Bejaoui M;Pantazi E;Calvo M;Folch-Puy E;Serafín A;Pasut G;Panisello A;Adam R;Roselló-Catafau J
通讯作者：
Roselló-Catafau J
鸢尾素通过抑制线粒体过度裂变、促进线粒体生物发生和减少氧化应激来减轻肝脏缺血再灌注损伤
影响因子：
11.4
作者：
Bi J;Zhang J;Ren Y;Du Z;Li Q;Wang Y;Wei S;Yang L;Zhang J;Liu C;Lv Y;Wu R
通讯作者：
Wu R
影响因子：
5.5
作者：
Belosludtsev, Konstantin N.;Dubinin, Mikhail V.;Belosludtseva, Natalia V.
通讯作者：
Belosludtseva, Natalia V.
影响因子：
4
作者：
Han, Yu-fang;Zhao, Yan-bing;Li, Zhong-dong
通讯作者：
Li, Zhong-dong
影响因子：
6
作者：
Belosludtsev, Konstantin N.;Talanov, Eugeny Yu;Belosludtseva, Natalia, V
通讯作者：
Belosludtseva, Natalia, V