Parkin and PINK1: much more than mitophagy

被引:390
作者
Scarffe, Leslie A. [1 ,2 ,3 ,7 ]
Stevens, Daniel A. [1 ,2 ,3 ]
Dawson, Valina L. [1 ,2 ,3 ,4 ,5 ,7 ]
Dawson, Ted M. [1 ,2 ,3 ,5 ,6 ,7 ]
机构
[1] Johns Hopkins Univ, Sch Med, Inst Cell Engn, Neuroregenerat Program, Baltimore, MD 21205 USA
[2] Johns Hopkins Univ, Sch Med, Inst Cell Engn, Stem Cell Program, Baltimore, MD 21205 USA
[3] Johns Hopkins Univ, Sch Med, Solomon H Snyder Dept Neurosci, Baltimore, MD 21205 USA
[4] Johns Hopkins Univ, Sch Med, Dept Physiol, Baltimore, MD 21205 USA
[5] Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21205 USA
[6] Johns Hopkins Univ, Sch Med, Dept Pharmacol & Mol Sci, Baltimore, MD 21205 USA
[7] Adrienne Hells Malvin Med Res Fdn, New Orleans, LA 70130 USA
基金
加拿大健康研究院;
关键词
REGULATES MITOCHONDRIAL DYNAMICS; COMPLEX-I; QUALITY-CONTROL; MITOFUSIN; DISEASE; DYSFUNCTION; MUTATIONS; NEURODEGENERATION; INTERACTS; PROMOTES;
D O I
10.1016/j.tins.2014.03.004
中图分类号
Q189 [神经科学];
学科分类号
071006 [神经生物学];
摘要
Parkinson's disease (PD) is a progressive neurodegenerative disease that causes a debilitating movement disorder. Although most cases of PD appear to be sporadic, rare Mendelian forms have provided tremendous insight into disease pathogenesis. Accumulating evidence suggests that impaired mitochondria underpin PD pathology. In support of this theory, data from multiple PD models have linked Phosphatase and tensin homolog (PTEN)-induced putative kinase 1 (PINK1) and parkin, two recessive PD genes, in a common pathway impacting mitochondrial health, prompting a flurry of research to identify their mitochondrial targets. Recent work has focused on the role of PINK1 and parkin in mediating mitochondria! autophagy (mitophagy); however, emerging evidence casts parkin and PINK1 as key players in multiple domains of mitochondrial health and quality control.
引用
收藏
页码:315 / 324
页数:10
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