Parkinson's Disease: A Complex Interplay of Mitochondrial DNA Alterations and Oxidative Stress

被引：49

作者：

Ciccone, Sarah ^{[1
]}

Maiani, Emiliano ^{[1
]}

Bellusci, Giovanna ^{[1
]}

Diederich, Marc ^{[2
,3
]}

Gonfloni, Stefania ^{[1
,2
]}

机构：

[1] Univ Roma Tor Vergata, Dept Biol, I-00133 Rome, Italy

[2] Kirchberg Hosp, Lab Biol Mol & Cellulaire Canc, L-2540 Luxembourg, Luxembourg

[3] Seoul Natl Univ, Coll Pharm, Seoul 151742, South Korea

来源：

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | 2013年 / 14卷 / 02期

关键词：

neurodegenerative diseases; Parkinson's disease (PD); base excision repair (BER); mitochondria; oxidative stress; reactive oxidative species (ROS); reactive nitrogen species (RNS); c-Abl; reduced glutathione (GSH); oxidized glutathione (GSS-); NUCLEOTIDE EXCISION-REPAIR; ABL TYROSINE KINASE; STRAND BREAK REPAIR; C-ABL; MOLECULAR-MECHANISMS; MAMMALIAN-CELLS; GENE-EXPRESSION; DAMAGE RESPONSE; PROTEIN; BRAIN;

D O I：

10.3390/ijms14022388

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Parkinson's disease (PD) is one of the most common age-related neurodegenerative diseases. This pathology causes a significant loss of dopaminergic neurons in the Substantia Nigra. Several reports have claimed a role of defective nuclear and mitochondrial DNA repair pathways in PD etiology, in particular, of the Base Excision Repair (BER) system. In addition, recent findings, related to PD progression, indicate that oxidative stress pathways involving c-Abl and GST could also be implicated in this pathology. This review focuses on recently described networks most likely involved in an integrated manner in the course of PD.

引用

页码：2388 / 2409

页数：22

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