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线粒体自噬的诱导与检测

Induction and Detection of Mitophagy.

作者信息

Yapryntseva Maria A, Zhivotovsky Boris, Gogvadze Vladimir

机构信息

Faculty of Basic Medicine, Lomonosov Moscow State University, Moscow, Russia.

Karolinska Institutet, Institute of Environmental Medicine, Stockholm, Sweden.

出版信息

Methods Mol Biol. 2022;2445:227-239. doi: 10.1007/978-1-0716-2071-7_14.

DOI:10.1007/978-1-0716-2071-7_14
PMID:34972995
Abstract

Mitophagy, a process of selective elimination of mitochondria by autophagy, is a mechanism of mitochondrial quality control that maintains mitochondrial network functionality. The elimination of damaged mitochondria through autophagy requires two steps: induction of general autophagy and priming of damaged mitochondria for selective autophagic recognition. Mitophagy impairment is linked to various pathologies; thus, removal of malfunctioning or even harmful mitochondria is vital to cellular physiology. Here, we describe methods that can be applied to the investigation of mitophagy.

摘要

线粒体自噬是一种通过自噬选择性清除线粒体的过程,是维持线粒体网络功能的线粒体质量控制机制。通过自噬清除受损线粒体需要两个步骤:诱导一般自噬和使受损线粒体启动以进行选择性自噬识别。线粒体自噬功能障碍与多种病理状况相关;因此,清除功能失调甚至有害的线粒体对细胞生理至关重要。在这里,我们描述了可应用于线粒体自噬研究的方法。

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1
Induction and Detection of Mitophagy.线粒体自噬的诱导与检测
Methods Mol Biol. 2022;2445:227-239. doi: 10.1007/978-1-0716-2071-7_14.
2
Mitochondrial morphology in mitophagy and macroautophagy.线粒体自噬和巨自噬中的线粒体形态
Biochim Biophys Acta. 2013 Jan;1833(1):205-12. doi: 10.1016/j.bbamcr.2012.02.012. Epub 2012 Mar 1.
3
Increased levels of reduced cytochrome b and mitophagy components are required to trigger nonspecific autophagy following induced mitochondrial dysfunction.在诱导线粒体功能障碍后,需要增加还原细胞色素 b 和线粒体自噬成分的水平以触发非特异性自噬。
J Cell Sci. 2013 Jan 15;126(Pt 2):415-26. doi: 10.1242/jcs.103713. Epub 2012 Dec 10.
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Monitoring selective autophagy of mitochondria using super-resolution microscopy.使用超分辨率显微镜监测线粒体的选择性自噬。
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Mitophagy is not induced by mitochondrial damage but plays a role in the regulation of cellular autophagic activity.线粒体自噬不是由线粒体损伤所诱导的,而是在细胞自噬活性的调节中发挥作用。
Autophagy. 2013 Nov 1;9(11):1897-9. doi: 10.4161/auto.23979. Epub 2013 May 3.
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Alternative macroautophagy and mitophagy.替代性巨自噬和线粒体自噬。
Int J Biochem Cell Biol. 2014 May;50:64-6. doi: 10.1016/j.biocel.2014.02.016. Epub 2014 Feb 22.
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Mitochondria autophagy is induced after hypoxic/ischemic stress in a Drp1 dependent manner: the role of inhibition of Drp1 in ischemic brain damage.线粒体自噬在缺氧/缺血应激后以依赖动力相关蛋白1(Drp1)的方式被诱导:Drp1抑制在缺血性脑损伤中的作用
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Mitophagy: Link to cancer development and therapy.线粒体自噬:与癌症发展和治疗的关联
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Oxidative stress-induced autophagy in plants: the role of mitochondria.植物中氧化应激诱导的自噬:线粒体的作用。
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Mitochondrial autophagy in neural function, neurodegenerative disease, neuron cell death, and aging.线粒体自噬在神经功能、神经退行性疾病、神经元细胞死亡和衰老中的作用。
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Characterization of immune features and immunotherapy response in subtypes of hepatocellular carcinoma based on mitophagy.基于线粒体自噬的肝细胞癌亚型免疫特征及免疫治疗反应的研究
Front Immunol. 2022 Oct 11;13:966167. doi: 10.3389/fimmu.2022.966167. eCollection 2022.

本文引用的文献

1
Molecular mechanisms of mitophagy and its roles in neurodegenerative diseases.线粒体自噬的分子机制及其在神经退行性疾病中的作用。
Pharmacol Res. 2021 Jan;163:105240. doi: 10.1016/j.phrs.2020.105240. Epub 2020 Oct 11.
2
A Healthy Heart and a Healthy Brain: Looking at Mitophagy.健康的心脏与健康的大脑:审视线粒体自噬。
Front Cell Dev Biol. 2020 May 6;8:294. doi: 10.3389/fcell.2020.00294. eCollection 2020.
3
FUN14 domain-containing 1 promotes breast cancer proliferation and migration by activating calcium-NFATC1-BMI1 axis.FUN14 结构域包含蛋白 1 通过激活钙-NFATC1-BMI1 轴促进乳腺癌的增殖和迁移。
EBioMedicine. 2019 Mar;41:384-394. doi: 10.1016/j.ebiom.2019.02.032. Epub 2019 Feb 23.
4
Hydrogen peroxide-induced mitophagy contributes to laryngeal cancer cells survival via the upregulation of FUNDC1.过氧化氢诱导的线粒体自噬通过上调 FUNDC1 促进喉癌细胞存活。
Clin Transl Oncol. 2019 May;21(5):596-606. doi: 10.1007/s12094-018-1958-5. Epub 2018 Oct 3.
5
High expression of FUNDC1 predicts poor prognostic outcomes and is a promising target to improve chemoradiotherapy effects in patients with cervical cancer.FUNDC1的高表达预示着预后不良,是改善宫颈癌患者放化疗效果的一个有前景的靶点。
Cancer Med. 2017 Aug;6(8):1871-1881. doi: 10.1002/cam4.1112. Epub 2017 Jul 18.
6
Mitophagy and Alzheimer's Disease: Cellular and Molecular Mechanisms.线粒体自噬与阿尔茨海默病:细胞和分子机制
Trends Neurosci. 2017 Mar;40(3):151-166. doi: 10.1016/j.tins.2017.01.002. Epub 2017 Feb 9.
7
Parkin and mitophagy in cancer.帕金森蛋白与癌症中的线粒体自噬
Oncogene. 2017 Mar;36(10):1315-1327. doi: 10.1038/onc.2016.302. Epub 2016 Sep 5.
8
Deciphering the Molecular Signals of PINK1/Parkin Mitophagy.解析 PINK1/Parkin 介导的线粒体自噬的分子信号
Trends Cell Biol. 2016 Oct;26(10):733-744. doi: 10.1016/j.tcb.2016.05.008. Epub 2016 Jun 10.
9
New method to assess mitophagy flux by flow cytometry.通过流式细胞术评估线粒体自噬通量的新方法。
Autophagy. 2015;11(5):833-43. doi: 10.1080/15548627.2015.1034403.
10
Mutational analysis of the PINK1 gene in early-onset parkinsonism in Europe and North Africa.欧洲和北非早发性帕金森病中PINK1基因的突变分析。
Brain. 2006 Mar;129(Pt 3):686-94. doi: 10.1093/brain/awl005. Epub 2006 Jan 9.