Department of Critical Care Medicine, Zhongnan Hospital of Wuhan University, Wuhan 430071, China.
Branch, Center for Cancer Research, National Cancer Institute, National Institutes of HealthNeuro-Oncology, Bethesda, Maryland, USA.
Autophagy. 2023 Feb;19(2):401-414. doi: 10.1080/15548627.2022.2084862. Epub 2022 Jun 9.
Mitophagy is an essential mitochondrial quality control mechanism that eliminates damaged mitochondria and the production of reactive oxygen species (ROS). The relationship between mitochondria oxidative stress, ROS production and mitophagy are intimately interwoven, and these processes are all involved in various pathological conditions of acute kidney injury (AKI). The elimination of damaged mitochondria through mitophagy in mammals is a complicated process which involves several pathways. Furthermore, the interplay between mitophagy and different types of cell death, such as apoptosis, pyroptosis and ferroptosis in kidney injury is unclear. Here we will review recent advances in our understanding of the relationship between ROS and mitophagy, the different mitophagy pathways, the relationship between mitophagy and cell death, and the relevance of these processes in the pathogenesis of AKI. AKI: acute kidney injury; AMBRA1: autophagy and beclin 1 regulator 1; ATP: adenosine triphosphate; BAK1: BCL2 antagonist/killer 1; BAX: BCL2 associated X, apoptosis regulator; BCL2: BCL2 apoptosis regulator; BECN1: beclin 1; BH3: BCL2 homology domain 3; BNIP3: BCL2 interacting protein 3; BNIP3L/NIX: BCL2 interacting protein 3 like; CASP1: caspase 1; CAT: catalase; CCCP: carbonyl cyanide m-chlorophenylhydrazone; CI-AKI: contrast-induced acute kidney injury; CISD1: CDGSH iron sulfur domain 1; CL: cardiolipin; CNP: 2',3'-cyclic nucleotide 3'-phosphodiesterase; DNM1L/DRP1: dynamin 1 like; E3: enzyme 3; ETC: electron transport chain; FA: folic acid; FUNDC1: FUN14 domain containing 1; G3P: glycerol-3-phosphate; G6PD: glucose-6-phosphate dehydrogenase; GPX: glutathione peroxidase; GSH: glutathione; GSK3B: glycogen synthase kinase 3 beta; GSR: glutathione-disulfide reductase; HIF1A: hypoxia inducible factor 1 subunit alpha; HUWE1: HECT, UBA and WWE domain containing 1; IL1B: interleukin 1 beta; IMM: inner mitochondrial membrane; IPC: ischemic preconditioning; IRI: ischemia-reperfusion injury; LIR: LC3-interacting region; LPS: lipopolysaccharide; MA: malate-aspartate; MPT: mitochondrial permeability transition; MUL1: mitochondrial E3 ubiquitin protein ligase 1; mtROS: mitochondrial ROS; NLR: NOD-like receptor; NLRP3: NLR family pyrin domain containing 3; NOX: NADPH oxidase; OGD-R: oxygen-glucose deprivation-reperfusion; OMM: outer mitochondrial membrane; OPA1: OPA1 mitochondrial dynamin like GTPase; OXPHOS: oxidative phosphorylation; PARL: presenilin associated rhomboid like; PINK1: PTEN induced kinase 1; PLSCR3: phospholipid scramblase 3; PMP: peptidase, mitochondrial processing; PRDX: peroxiredoxin; PRKN: parkin RBR E3 ubiquitin protein ligase; RPTC: rat proximal tubular cells; ROS: reactive oxygen species; SLC7A11/xCT: solute carrier family 7 member 11; SOD: superoxide dismutase; SOR: superoxide reductase; SQSTM1/p62: sequestosome 1; TCA: tricarboxylic acid; TIMM: translocase of inner mitochondrial membrane; TOMM: translocase of outer mitochondrial membrane; TXN: thioredoxin; VDAC: voltage dependent anion channel; VCP: valosin containing protein.
自噬是一种重要的线粒体质量控制机制，可消除受损的线粒体和活性氧物质（ROS）的产生。线粒体氧化应激、ROS 产生和自噬之间的关系是密切交织的，这些过程都涉及到急性肾损伤（AKI）的各种病理情况。哺乳动物通过自噬消除受损的线粒体是一个复杂的过程，涉及几种途径。此外，自噬与不同类型的细胞死亡（如肾损伤中的细胞凋亡、焦亡和铁死亡）之间的相互作用尚不清楚。在这里，我们将回顾近年来对 ROS 与自噬、不同自噬途径、自噬与细胞死亡之间关系的理解的最新进展，以及这些过程在 AKI 发病机制中的相关性。AKI：急性肾损伤；AMBRA1：自噬和 beclin 1 调节因子 1；ATP：三磷酸腺苷；BAK1：BCL2 拮抗剂/杀手 1；BAX：BCL2 相关 X，凋亡调节剂；BCL2：BCL2 凋亡调节剂；BECN1：beclin 1；BH3：BCL2 同源结构域 3；BNIP3：BCL2 相互作用蛋白 3；BNIP3L/NIX：BCL2 相互作用蛋白 3 样；CASP1：半胱氨酸天冬氨酸蛋白酶 1；CAT：过氧化氢酶；CCCP：羰基氰化物 m-氯苯腙；CI-AKI：对比剂诱导的急性肾损伤；CISD1：CDGSH 铁硫域 1；CL：心磷脂；CNP：2'，3'-环核苷酸 3'-磷酸二酯酶；DNM1L/DRP1：动力蛋白 1 样；E3：酶 3；ETC：电子传递链；FA：叶酸；FUNDC1：FUN14 结构域包含 1；G3P：甘油-3-磷酸；G6PD：葡萄糖-6-磷酸脱氢酶；GPX：谷胱甘肽过氧化物酶；GSH：谷胱甘肽；GSK3B：糖原合酶激酶 3β；GSR：谷胱甘肽-二硫化物还原酶；HIF1A：缺氧诱导因子 1 亚单位α；HUWE1：HECT、UBA 和 WWE 结构域包含 1；IL1B：白细胞介素 1β；IMM：内线粒体膜；IPC：缺血预处理；IRI：缺血再灌注损伤；LIR：LC3 相互作用区；LPS：脂多糖；MA：苹果酸-天冬氨酸；MPT：线粒体通透性转换；MUL1：线粒体 E3 泛素蛋白连接酶 1；mtROS：线粒体 ROS；NLR：NOD 样受体；NLRP3：NLR 家族吡咯烷域包含 3；NOX：NADPH 氧化酶；OGD-R：氧-葡萄糖剥夺-再灌注；OMM：外线粒体膜；OPA1：OPA1 线粒体动力蛋白样 GTPase；OXPHOS：氧化磷酸化；PARL：早老素相关环指蛋白；PINK1：PTEN 诱导的激酶 1；PLSCR3：磷脂酶 scramblase 3；PMP：肽酶，线粒体加工；PRDX：过氧化物酶；PRKN：帕金森病 RBR E3 泛素蛋白连接酶；RPTC：大鼠近端肾小管细胞；ROS：活性氧物质；SLC7A11/xCT：溶质载体家族 7 成员 11；SOD：超氧化物歧化酶；SOR：超氧化物还原酶；SORT1：分选连接蛋白 1；SQSTM1/p62：自噬体 1；TCA：三羧酸；TIMM：线粒体内膜转运蛋白；TOMM：线粒体外膜转运蛋白；TXN：硫氧还蛋白；VDAC：电压依赖性阴离子通道；VCP：包含 valosin 的蛋白。
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