The DOI matches its Crossref record; 31 of the 31 references it cites were found in a registry or an index.
Mitochondrial dynamics-fusion, fission, movement, and mitophagy-in neurodegenerative diseases
Open accessAbstract
Neurons are metabolically active cells with high energy demands at locations distant from the cell body. As a result, these cells are particularly dependent on mitochondrial function, as reflected by the observation that diseases of mitochondrial dysfunction often have a neurodegenerative component. Recent discoveries have highlighted that neurons are reliant particularly on the dynamic properties of mitochondria. Mitochondria are dynamic organelles by several criteria. They engage in repeated cycles of fusion and fission, which serve to intermix the lipids and contents of a population of mitochondria. In addition, mitochondria are actively recruited to subcellular sites, such as the axonal and dendritic processes of neurons. Finally, the quality of a mitochondrial population is maintained through mitophagy, a form of autophagy in which defective mitochondria are selectively degraded. We review the general features of mitochondrial dynamics, incorporating recent findings on mitochondrial fusion, fission, transport and mitophagy. Defects in these key features are associated with neurodegenerative disease. Charcot-Marie-Tooth type 2A, a peripheral neuropathy, and dominant optic atrophy, an inherited optic neuropathy, result from a primary deficiency of mitochondrial fusion. Moreover, several major neurodegenerative diseases--including Parkinson's, Alzheimer's and Huntington's disease--involve disruption of mitochondrial dynamics. Remarkably, in several disease models, the manipulation of mitochondrial fusion or fission can partially rescue disease phenotypes. We review how mitochondrial dynamics is altered in these neurodegenerative diseases and discuss the reciprocal interactions between mitochondrial fusion, fission, transport and mitophagy.
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Citations
Cites
Parkin is recruited selectively to impaired mitochondria and promotes their autophagy
Narendra, D., Tanaka, A., Suen, D.-F., & Youle, R. J. (2008) · The Journal of Cell Biology · doi:10.1083/jcb.200809125 · Cited by 4,026
Fission and selective fusion govern mitochondrial segregation and elimination by autophagy
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Self-citationMitofusin 2 tethers endoplasmic reticulum to mitochondria
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Drosophila pink1 is required for mitochondrial function and interacts genetically with parkin
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Mitochondrial dysfunction in Drosophila PINK1 mutants is complemented by parkin
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OPA1 Controls Apoptotic Cristae Remodeling Independently from Mitochondrial Fusion
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Mutations in the mitochondrial GTPase mitofusin 2 cause Charcot-Marie-Tooth neuropathy type 2A
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“neuropathy affecting sensory and motor neurons of the distal extremities (8).”
BackgroundSelective degradation of mitochondria by mitophagy
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Disruption of Fusion Results in Mitochondrial Heterogeneity and Dysfunction
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“Potential answers include differential expression patterns between Mfn2 versus OPA1, functional differences between OPA1 (11) and Mfn2 (12), differences in an outer membrane fusion defect versus an inner membrane fusion defect (4) and redundancy between Mfn1 and Mfn2 (6,13).”
BackgroundInfluentialSelf-citation
Cited by
Mitochondrial dynamics in health and disease: mechanisms and potential targets
Chen, W., Zhao, H., & Li, Y. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01547-9 · Cited by 1,306
Fusion and fission: interlinked processes critical for mitochondrial health
Chan, D. C. (2012) · Annual Review of Genetics · doi:10.1146/annurev-genet-110410-132529 · Cited by 1,196
An Actin-Dependent Step in Mitochondrial Fission Mediated by the ER-Associated Formin INF2
Korobova, F., Ramabhadran, V., & Higgs, H. N. (2013) · Science · doi:10.1126/science.1228360 · Cited by 817
Mitochondrial Dysfunction and Oxidative Stress in Alzheimer’s Disease
Misrani, A., Tabassum, S., & Yang, L. (2021) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2021.617588 · Cited by 654
Mitochondrial optic neuropathies—Disease mechanisms and therapeutic strategies
Yu-Wai-Man, P., Griffiths, P. G., & Chinnery, P. F. (2011) · Progress in Retinal and Eye Research · doi:10.1016/j.preteyeres.2010.11.002 · Cited by 633
Metadata
- Authors
- Chen, H., & Chan, D. C.
- Venue
- Human Molecular Genetics
- Publisher
- Oxford University Press (OUP)
- Published
- 2009-10-06
- Volume
- 18
- Issue
- R2
- Pages
- R169-R176
- ISSN
- 0964-6906 (ISSN-L)
- 1460-2083
- OpenAlex
- W2105043890
- Cited by
- 1,458
- References
- 31
- FWCI
- 30.37
- Type
- journal article
- Language
- en
- Open access
- hybrid
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