Ubiquitin-mediated mitochondrial regulation by MITOL/MARCHF5 at a glance
Ubiquitin-mediated mitochondrial regulation by MITOL/MARCHF5 at a glance
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MITOL/MARCHF5 泛素介导的线粒体调节概览
DOI：
10.1093/jb/mvac092
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发表时间：
2022
期刊：
影响因子：
--
通讯作者：
Yanagi Shigeru
中科院分区：
文献类型：
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作者：
Nagashima Shun;Ito Naoki;Shiiba Isshin;Shimura Hiroki;Yanagi Shigeru
线粒体参与各种细胞过程，如能量产生、炎症反应和细胞死亡。线粒体功能障碍与许多与年龄相关的疾病有关，包括神经系统疾病和心力衰竭。线粒体的质量由线粒体动力学严格维持，线粒体动力学与来自内质网（ER）的磷脂和其他物质的充足供应有关。位于线粒体外膜的E3泛素连接酶MITOL/MARCHF 5通过调节线粒体动力学、形成线粒体-ER接触和线粒体自噬来负责线粒体质量控制。MITOL缺乏已被证明会损害线粒体功能，导致过度的炎症反应，并增加对压力的脆弱性，导致疾病的恶化。本文就MITOL对线粒体功能的调节及其与疾病的关系作一综述。
Mitochondria are involved in various cellular processes, such as energy production, inflammatory responses and cell death. Mitochondrial dysfunction is associated with many age-related diseases, including neurological disorders and heart failure. Mitochondrial quality is strictly maintained by mitochondrial dynamics linked to an adequate supply of phospholipids and other substances from the endoplasmic reticulum (ER). The outer mitochondrial membrane-localized E3 ubiquitin ligase MITOL/MARCHF5 is responsible for mitochondrial quality control through the regulation of mitochondrial dynamics, formation of mitochondria-ER contacts and mitophagy. MITOL deficiency has been shown to impair mitochondrial function, cause an excessive inflammatory response and increase vulnerability to stress, resulting in the exacerbation of the disease. In this study, we overview the ubiquitin-mediated regulation of mitochondrial function by MITOL and the relationship between MITOL and diseases.