Sending Out an SOS: Mitochondria as a Signaling Hub.

Sending Out an SOS: Mitochondria as a Signaling Hub.
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DOI:
10.3389/fcell.2016.00109
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发表时间:
2016
影响因子:
5.5
通讯作者:
Khalimonchuk O
Khalimonchuk O
中科院分区:
生物学2区
文献类型:
--
作者:
Bohovych I;Khalimonchuk O

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正常的细胞生理学严重依赖于许多线粒体活动,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。过去二十年来线粒体研究的进展提供了坚实的证据,证明这些细胞器与细胞的其他部分深度整合,并且有多种机制可以监测和传达线粒体的功能状态。然而,在许多情况下,各种细胞间通讯途径的确切分子性质才刚刚开始出现。在这里,我们回顾了由受损或功能失调的线粒体发出的各种信号,以及响应于这些信号而激活的应激反应途径,以恢复线粒体功能并促进细胞存活。
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.
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