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PMID: 21146459 Published · ppublish English Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. Review

Mitophagy: the latest problem for Parkinson's disease.

Trends in molecular medicine ·Vol. 17 ·No. 3 ·2011-03-00 ·Pages 158-65

Vives-Bauza C, Przedborski S

Abstract

Parkinson's disease (PD) is a common neurodegenerative disorder of unknown cause. Some familial forms of PD are provoked by mutations in the genes encoding for the PTEN (phosphatase and tensin homolog)-induced putative kinase-1 (PINK1) and Parkin. Mounting evidence indicates that PINK1 and Parkin might function in concert to modulate mitochondrial degradation, termed mitophagy. However, the molecular mechanisms by which PINK1/Parkin affect mitophagy are just beginning to be elucidated. Herein, we review the main advances in our understanding of the PINK1/Parkin pathway. Because of the phenotypic similarities among the different forms of PD, a better understanding of PINK1/Parkin biology might have far-reaching pathogenic and therapeutic implications for both the inherited and the sporadic forms of PD.

MeSH Terms
Animals Autophagy Humans Mitochondria/enzymology,genetics,metabolism Parkinson Disease/enzymology,genetics,physiopathology Protein Kinases/genetics,metabolism Ubiquitin-Protein Ligases/genetics,metabolism
Chemicals
Ubiquitin-Protein Ligases parkin protein Protein Kinases PTEN-induced putative kinase
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Vives-Bauza Cristofol
Department of Neurology, Columbia University, New York, NY, USA.
Przedborski Serge
Article Info
Journal
Trends in molecular medicine
Abbr.
Trends Mol Med
ISSN
1471-499X
Published
2011-03-00
Epub
2010-00-09
Pages
158-65
Language
English
Region
England
NLM ID
100966035
Subset
IM
Grants
NIA NIH HHS · AG021617 · United States
NINDS NIH HHS · NS042269 · United States
NINDS NIH HHS · NS062180 · United States
NINDS NIH HHS · NS064191 · United States
NINDS NIH HHS · NS38370 · United States
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