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神经退行性变和细菌感染中的线粒体自噬与线粒体未折叠蛋白反应

Mitophagy and the mitochondrial unfolded protein response in neurodegeneration and bacterial infection.

作者信息

Pellegrino Mark W, Haynes Cole M

出版信息

BMC Biol. 2015 Apr 3;13:22. doi: 10.1186/s12915-015-0129-1.

Abstract

Mitochondria are highly dynamic and structurally complex organelles that provide multiple essential metabolic functions. Mitochondrial dysfunction is associated with neurodegenerative conditions such as Parkinson's disease, as well as bacterial infection. Here, we explore the roles of mitochondrial autophagy (mitophagy) and the mitochondrial unfolded protein response (UPR(mt)) in the response to mitochondrial dysfunction, focusing in particular on recent evidence on the role of mitochondrial import efficiency in the regulation of these stress pathways and how they may interact to protect the mitochondrial pool while initiating an innate immune response to protect against bacterial pathogens.

摘要

线粒体是高度动态且结构复杂的细胞器,具有多种重要的代谢功能。线粒体功能障碍与帕金森病等神经退行性疾病以及细菌感染有关。在此,我们探讨线粒体自噬(mitophagy)和线粒体未折叠蛋白反应(UPR(mt))在应对线粒体功能障碍中的作用,特别关注线粒体导入效率在调节这些应激途径中的作用的最新证据,以及它们如何相互作用以保护线粒体库,同时启动先天性免疫反应以抵御细菌病原体。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34ec/4384303/0749ce13d67e/12915_2015_129_Fig1_HTML.jpg

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