Regulation by mitophagy
Regulation by mitophagy
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DOI：
10.1016/j.biocel.2014.05.012
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发表时间：
2014-08-01
影响因子：
4
通讯作者：
Imai, Yuzuru
中科院分区：
文献类型：
--
作者：
Hattori, Nobutaka;Saiki, Shinji;Imai, Yuzuru
真核生物采用精细的线粒体质量控制来维持发电细胞器的功能。线粒体质量控制对于神经和肌肉组织的维持特别重要。线粒体自噬是自噬途径的特殊版本。线粒体自噬将受损的线粒体递送至溶酶体进行降解。最近，一系列优雅的研究表明，两个帕金森病相关基因PINK 1和parkin参与维持健康的线粒体作为线粒体自噬。Parkin与PINK 1合作，特异性识别线粒体膜电位降低（Delta psi m）的受损线粒体，快速将其从线粒体网络中分离出来，并通过泛素-蛋白酶体和自噬途径消除它们。在这里，我们介绍和审查最近的研究，有助于了解线粒体自噬的分子机制，如PINK 1和帕金森介导的线粒体调控。我们还讨论了PINK 1-Parkin通路的缺陷如何导致帕金森病的神经退行性变。(C)2014爱思唯尔有限公司版权所有。
Eukaryotes employ elaborate mitochondrial quality control to maintain the function of the power-generating organelle. Mitochondrial quality control is particularly important for the maintenance of neural and muscular tissues. Mitophagy is specialized version of the autophagy pathway. Mitophagy delivers damaged mitochondria to lysosomes for degradation. Recently, a series of elegant studies have demonstrated that two Parkinson's disease-associated genes PINK1 and parkin are involved in the maintenance of healthy mitochondria as mitophagy. Parkin in co-operation with PINK1 specifically recognizes damaged mitochondria with reduced mitochondrial membrane potential (Delta psi m), rapidly isolates them from the mitochondrial network and eliminates them through the ubiquitin-proteasome and autophagy pathways. Here we introduce and review recent studies that contribute to understanding the molecular mechanisms of mitophagy such as PINK1 and Parkin-mediated mitochondrial regulation. We also discuss how defects in the PINK1-Parkin pathway may cause neurodegeneration in Parkinson's disease. (C) 2014 Elsevier Ltd. All rights reserved.