跨组织线粒体应激信号交流调控机体衰老研究进展

doi:10.16288/j.yczz.22-416

遗传 ›› 2023, Vol. 45 ›› Issue (3): 187-197.doi: 10.16288/j.yczz.22-416

跨组织线粒体应激信号交流调控机体衰老研究进展

张茜¹(), 王子豪^1,²(), 田烨^1,²()

1.中国科学院遗传与发育生物学研究所，分子发育生物学国家重点实验室，北京 100101
2.中国科学院大学，北京 100093

收稿日期:2022-12-21 修回日期:2023-01-30 出版日期:2023-03-20 发布日期:2023-02-24
通讯作者: 田烨 E-mail:zhangqian@genetics.ac.cn;wangzihao@genetics.ac.cn;ytian@genetics.ac.cn
作者简介:张茜，博士，研究方向：线粒体未折叠蛋白反应的跨组织调控。E-mail: zhangqian@genetics.ac.cn张茜，2015—2021年就读于中国科学院遗传与发育生物学研究所，在线粒体应激与衰老研究组攻读博士学位，目前在遗传发育所做博士后。博士期间主要研究跨组织线粒体应激的调控机制，发现了Wnt信号介导机体整体的线粒体蛋白稳态以及衰老调控(Cell，2018年)，发现了一个全新的跨代遗传现象——神经元的线粒体应激通过神经与生殖腺的信号交流，诱导后代继承线粒体未折叠蛋白反应，使后代具有更强的抗逆能力和更长的寿命(Nature Cell Biology，2021年)。这些工作解析了线粒体应激的跨组织和跨世代调控机制，推动了该前沿领域的发展。博士论文《Wnt信号通路介导细胞非自主性线粒体未折叠蛋白反应》获得2021年中国科学院优秀博士学位论文。|王子豪，在读博士研究生，研究方向：细胞非自主性线粒体未折叠蛋白反应的调控机制。E-mail: wangzihao@genetics.ac.cn;
张茜和王子豪并列第一作者。
基金资助:
国家自然科学基金项目(32200624);，博士后创新人才支持计划(BX2021356);博士后面上项目(2021M703474)

Inter-tissue communication of mitochondrial stress in aging

Qian Zhang¹(), Zihao Wang^1,²(), Ye Tian^1,²()

1. State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China
2. University of Chinese Academy of Sciences, Beijing 100093, China

Received:2022-12-21 Revised:2023-01-30 Online:2023-03-20 Published:2023-02-24
Contact: Tian Ye E-mail:zhangqian@genetics.ac.cn;wangzihao@genetics.ac.cn;ytian@genetics.ac.cn
Supported by:
the National Natural Science Foundation of China(32200624);the China National Postdoctoral Program for Innovative Talents(BX2021356);the China Postdoctoral Science Foundation Funded Project(2021M703474)

摘要/Abstract

摘要：

线粒体内蛋白质稳态的平衡对于细胞正常的生理功能非常关键。线粒体蛋白稳态失衡时，细胞会启动应激反应机制，即线粒体未折叠蛋白反应(mitochondrial unfolded protein response，UPR^mt)，修复线粒体功能，平衡细胞内稳态。尽管线粒体的严重损伤对机体是有害的，但在线虫(Caenorhabditis elegans)、果蝇(Drosophila melanogaste)及小鼠(Mus musculus)中都有研究表明线粒体的轻微损伤可以通过激活UPR^mt，促进寿命延长。有趣的是，在没有直接经历线粒体损伤的细胞或组织中，UPR^mt也能以非自主方式被诱导。不同组织间可以通过名为“mitokine”的细胞因子进行UPR^mt的跨组织调控，系统性地协调机体整体的压力适应能力和抗衰老能力。该调控机制与衰老相关神经退行性疾病、癌症等多种疾病密切相关，近年来有关研究与日俱增。本文系统总结了线粒体应激及其组织间通讯的机制，并介绍了跨组织线粒体应激交流信号“mitokine”调控衰老进程的最新研究进展，以期为跨组织信号调控和机体衰老等研究提供参考。

关键词: 线粒体未折叠蛋白反应, 蛋白稳态, 跨组织调控, 衰老

Abstract:

The protein homeostasis in mitochondria is critical for the normal physiological function of cells. To cope with mitochondrial stress, cells elicit specific stress response named mitochondrial unfolded protein response (UPR^mt), to maintain mitochondrial homeostasis and repair mitochondrial function. Although severe damage to mitochondria is detrimental, studies in worms, flies, and mice have shown that mild mitochondrial damage promotes longevity by activating UPR^mt. Interestingly, UPR^mt can also be induced in a cell non-autonomous manner in cells or tissues which are not directly experiencing mitochondrial stress. The secreted molecules called “mitokine” are responsible for the mitochondrial stress communication between different tissues. This inter-tissue regulation of mitochondrial stress response systematically coordinates the adaptation ability which is closely associated with aging and a variety of diseases such as neurodegeneration and cancer. In this review, we summarize recent advances about inter-tissue mitochondrial stress communications, and introduce the current knowledge about the “mitokine” and its regulation on aging for further studies.

Key words: mitochondrial unfolded protein response, protein homeostasis, inter-tissue regulation, aging

张茜, 王子豪, 田烨. 跨组织线粒体应激信号交流调控机体衰老研究进展[J]. 遗传, 2023, 45(3): 187-197.

Qian Zhang, Zihao Wang, Ye Tian. Inter-tissue communication of mitochondrial stress in aging[J]. Hereditas(Beijing), 2023, 45(3): 187-197.

图/表 1

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跨组织线粒体应激信号交流调控机体衰老研究进展

Inter-tissue communication of mitochondrial stress in aging

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