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Parkinson’s Disease
Volume 2016, Article ID 2613401, 7 pages
Review Article

Chaperone-Mediated Autophagy and Mitochondrial Homeostasis in Parkinson’s Disease

1Department of Neurosurgery, Tangdu Hospital, The Fourth Military Medical University, 569 Xinsi Road, Xi’an, Shaanxi 710038, China
2Department of Pharmacology and Neurology, School of Medicine, Emory University, Atlanta, GA 30322, USA

Received 27 December 2015; Revised 4 April 2016; Accepted 29 May 2016

Academic Editor: Matthew Gegg

Copyright © 2016 Ruixin Yang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Parkinson’s disease (PD), a complex neurodegenerative disorder, is pathologically characterized by the formation of Lewy bodies and loss of dopaminergic neurons in the substantia nigra pars compacta (SNc). Mitochondrial dysfunction is considered to be one of the most important causative mechanisms. In addition, dysfunction of chaperone-mediated autophagy (CMA), one of the lysosomal proteolytic pathways, has been shown to play an important role in the pathogenesis of PD. An exciting and important development is recent finding that CMA and mitochondrial quality control may be linked. This review summarizes the studies revealing the link between autophagy and mitochondrial function. Discussions are focused on the connections between CMA and mitochondrial failure and on the role of MEF2D, a neuronal survival factor, in mediating the regulation of mitochondria in the context of CMA. These new findings highlight the need to further explore the possibility of targeting the MEF2D-mitochondria-CMA network in both understanding the PD pathogenesis and developing novel therapeutic strategies.