PINK1 import regulation; a fine system to convey mitochondrial stress to the cytosol.

PINK1 import regulation; a fine system to convey mitochondrial stress to the cytosol.
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DOI:
10.1186/s12915-017-0470-7
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发表时间:
2018-01-10
期刊:
影响因子:
5.4
通讯作者:
Youle RJ
Youle RJ
中科院分区:
生物学2区
文献类型:
--
作者:
Sekine S;Youle RJ

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从遗传性帕金森病的见解表明,线粒体自噬不足可能是疾病的病因之一。PINK 1/Parkin依赖性线粒体自噬有助于维持健康的线粒体网络,它是通过激活受损线粒体上特异性的PINK 1激酶而启动的。最近对这一过程的研究表明,PINK 1进入线粒体的输入受到调节,并产生了一种应激传感机制。在这篇综述中,我们专注于线粒体应激依赖性PINK 1激活的机制,通过调节PINK 1进入不同的线粒体区室,以及这如何提供策略来重新激活PINK 1/Parkin通路。
Insights from inherited forms of parkinsonism suggest that insufficient mitophagy may be one etiology of the disease. PINK1/Parkin-dependent mitophagy, which helps maintain a healthy mitochondrial network, is initiated by activation of the PINK1 kinase specifically on damaged mitochondria. Recent investigation of this process reveals that import of PINK1 into mitochondria is regulated and yields a stress-sensing mechanism. In this review, we focus on the mechanisms of mitochondrial stress-dependent PINK1 activation that is exerted by regulated import of PINK1 into different mitochondrial compartments and how this offers strategies to pharmacologically activate the PINK1/Parkin pathway.
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