Fiorese Christopher J, Haynes Cole M
a Department of Molecular Cell and Cancer Biology , University of Massachusetts Medical School , Worcester , MA , USA.
b BCMB Allied Program , Weill Cornell Medical College , New York , NY , USA.
Crit Rev Biochem Mol Biol. 2017 Jun;52(3):304-313. doi: 10.1080/10409238.2017.1291577. Epub 2017 Feb 22.
Mitochondrial function is central to many different processes in the cell, from oxidative phosphorylation to the synthesis of iron-sulfur clusters. Therefore, mitochondrial dysfunction underlies a diverse array of diseases, from neurodegenerative diseases to cancer. Stress can be communicated to the cytosol and nucleus from the mitochondria through many different signals, and in response the cell can effect everything from transcriptional to post-transcriptional responses to protect the mitochondrial network. How these responses are coordinated have only recently begun to be understood. In this review, we explore how the cell maintains mitochondrial function, focusing on the mitochondrial unfolded protein response (UPR), a transcriptional response that can activate a wide array of programs to repair and restore mitochondrial function.
线粒体功能对于细胞内许多不同过程至关重要，从氧化磷酸化到铁硫簇的合成。因此，线粒体功能障碍是多种疾病的基础，从神经退行性疾病到癌症。应激可通过多种不同信号从线粒体传递至细胞质和细胞核，作为响应，细胞可以产生从转录到转录后反应的各种效应，以保护线粒体网络。这些反应如何协调直到最近才开始被理解。在这篇综述中，我们探讨细胞如何维持线粒体功能，重点关注线粒体未折叠蛋白反应（UPR），这是一种转录反应，可激活一系列程序来修复和恢复线粒体功能。
