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帕金森病中自噬与线粒体功能的失调

Dysregulation of autophagy and mitochondrial function in Parkinson's disease.

作者信息

Wang Bao, Abraham Neeta, Gao Guodong, Yang Qian

机构信息

Department of Neurosurgery, Tangdu Hospital, The Fourth Military Medical University, No. 569 Xinsi Road, Baqiao District, Xi'an, 710038 Shaanxi Province China ; Department of Neurology, Beth Isreal Deaconess Medical Center, Harvard Medical School, 330 Brookline Ave, Boston, 02215 MA USA.

Department of Neurology, Beth Isreal Deaconess Medical Center, Harvard Medical School, 330 Brookline Ave, Boston, 02215 MA USA.

出版信息

Transl Neurodegener. 2016 Oct 31;5:19. doi: 10.1186/s40035-016-0065-1. eCollection 2016.

Abstract

Parkinson's disease (PD) is the second most common neurodegenerative disease. Increasing evidence supports that dysregulation of autophagy and mitochondrial function are closely related with PD pathogenesis. In this review, we briefly summarized autophagy pathway, which consists of macroautophagy, microautophagy and chaperone-mediated autophagy (CMA). Then, we discussed the involvement of mitochondrial dysfunction in PD pathogenesis. We specifically reviewed the recent developments in the relationship among several PD related genes, autophagy and mitochondrial dysfunction, followed by the therapeutic implications of these pathways. In conclusion, we propose that autophagy activity and mitochondrial homeostasis are of high importance in the pathogenesis of PD. Better understanding of these pathways can shed light on the novel therapeutic methods for PD prevention and amelioration.

摘要

帕金森病(PD)是第二常见的神经退行性疾病。越来越多的证据支持自噬和线粒体功能失调与PD发病机制密切相关。在本综述中,我们简要总结了自噬途径,其包括巨自噬、微自噬和伴侣介导的自噬(CMA)。然后,我们讨论了线粒体功能障碍在PD发病机制中的作用。我们特别回顾了几个与PD相关基因、自噬和线粒体功能障碍之间关系的最新进展,以及这些途径的治疗意义。总之,我们提出自噬活性和线粒体稳态在PD发病机制中至关重要。更好地理解这些途径可为预防和改善PD的新治疗方法提供线索。

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