Mitochondrial Fusion/Fission, Transport and Autophagy in Parkinson's Disease: When Mitochondria Get Nasty

被引:47
作者
Arduino, Daniela M. [1 ]
Raquel Esteves, A. [1 ]
Cardoso, Sandra M. [1 ,2 ]
机构
[1] Univ Coimbra, Ctr Neurosci & Cell Biol CNC, P-3004517 Coimbra, Portugal
[2] Univ Coimbra, Fac Med, P-3004517 Coimbra, Portugal
关键词
DOPAMINERGIC NEURON DEGENERATION; AXONAL PROTEIN-SYNTHESIS; ALPHA-SYNUCLEIN; COMPLEX-I; PINK1/PARKIN-MEDIATED MITOPHAGY; SPORADIC PARKINSONS; MOLECULAR MACHINERY; ENZYME-ACTIVITIES; OXIDATIVE STRESS; PINK1; FUNCTION;
D O I
10.4061/2011/767230
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Understanding the molecular basis of Parkinson's disease (PD) has proven to be a major challenge in the field of neurodegenerative diseases. Although several hypotheses have been proposed to explain the molecular mechanisms underlying the pathogenesis of PD, a growing body of evidence has highlighted the role of mitochondrial dysfunction and the disruption of the mechanisms of mitochondrial dynamics in PD and other parkinsonian disorders. In this paper, we comment on the recent advances in how changes in the mitochondrial function and mitochondrial dynamics (fusion/fission, transport, and clearance) contribute to neurodegeneration, specifically focusing on PD. We also evaluate the current controversies in those issues and discuss the role of fusion/fission dynamics in the mitochondrial lifecycle and maintenance. We propose that cellular demise and neurodegeneration in PD are due to the interplay between mitochondrial dysfunction, mitochondrial trafficking disruption, and impaired autophagic clearance.
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页数:13
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