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

被引:69
|
作者
Pellegrino, Mark W. [1 ]
Haynes, Cole M. [1 ,2 ]
机构
[1] Mem Sloan Kettering Canc Ctr, Cell Biol Program, New York, NY 10065 USA
[2] Weill Cornell Med Coll, BCMB Allied Program, New York, NY 10065 USA
基金
美国国家卫生研究院;
关键词
RESPIRATORY-CHAIN; TRANSLATIONAL INHIBITION; CAENORHABDITIS-ELEGANS; TARGETS MITOCHONDRIA; QUALITY-CONTROL; PARKIN; PINK1; UBIQUITIN; MUTATIONS; IMPORT;
D O I
10.1186/s12915-015-0129-1
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
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 (UPRmt) 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.
引用
收藏
页数:9
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