Bohovych Iryna, Khalimonchuk Oleh
Department of Biochemistry, University of Nebraska-Lincoln Lincoln, NE, USA.
Department of Biochemistry, University of Nebraska-LincolnLincoln, NE, USA; Nebraska Redox Biology Center, University of Nebraska-LincolnLincoln, NE, USA; Fred and Pamela Buffett Cancer Center, University of Nebraska Medical CenterOmaha, NE, USA.
Front Cell Dev Biol. 2016 Oct 13;4:109. doi: 10.3389/fcell.2016.00109. eCollection 2016.
Normal cellular physiology is critically dependent on numerous mitochondrial activities including energy conversion, cofactor and precursor metabolite synthesis, and regulation of ion and redox homeostasis. Advances in mitochondrial research during the last two decades provide solid evidence that these organelles are deeply integrated with the rest of the cell and multiple mechanisms are in place to monitor and communicate functional states of mitochondria. In many cases, however, the exact molecular nature of various mitochondria-to-cell communication pathways is only beginning to emerge. Here, we review various signals emitted by distressed or dysfunctional mitochondria and the stress-responsive pathways activated in response to these signals in order to restore mitochondrial function and promote cellular survival.
正常细胞生理学严重依赖于众多线粒体活动,包括能量转换、辅因子和前体代谢物合成,以及离子和氧化还原稳态的调节。过去二十年线粒体研究的进展提供了确凿证据,表明这些细胞器与细胞的其他部分深度整合,并且存在多种机制来监测和传递线粒体的功能状态。然而,在许多情况下,各种线粒体与细胞通讯途径的确切分子本质才刚刚开始显现。在这里,我们综述了受损或功能失调的线粒体发出的各种信号,以及为了恢复线粒体功能和促进细胞存活而响应这些信号激活的应激反应途径。