Mitochondrial Dynamics and Its Involvement in Disease
Abstract
The dynamic properties of mitochondria—including their fusion, fission, and degradation—are critical for their optimal function in energy generation. The interplay of fusion and fission confers widespread benefits on mitochondria, including efficient transport, increased homogenization of the mitochondrial population, and efficient oxidative phosphorylation. These benefits arise through control of morphology, content exchange, equitable inheritance of mitochondria, maintenance of high-quality mitochondrial DNA, and segregation of damaged mitochondria for degradation. The key components of the machinery mediating mitochondrial fusion and fission belong to the dynamin family of GTPases that utilize GTP hydrolysis to drive mechanical work on biological membranes. Defects in this machinery cause a range of diseases that especially affect the nervous system. In addition, several common diseases, including neurodegenerative diseases and cancer, strongly affect mitochondrial dynamics.
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Fusion ameliorates stress by mixing the contents of partially damaged mitochondria as a form of complementation, whereas fission is thought to induce oxidative stress and cell apoptosis.
“Fusion ameliorates stress by mixing the contents of partially damaged mitochondria as a form of complementation, whereas fission is thought to induce oxidative stress and cell apoptosis [33].”
From A High-Fat Diet Induces Muscle Mitochondrial Dysfunction and Impairs Swimming Capacity in Zebrafish: A New Model of Sarcopenic Obesity (2022) · cites this paper as [33]
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The Mitochondrial Fission Receptor MiD51 Requires ADP as a Cofactor
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Mitochondrial fusion and fission: The fine‐tune balance for cellular homeostasis
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- Authors
- Chan, D. C.
- Affiliations
- California Institute of Technology (US)
- Corresponding author
- Chan, David C.
- ORCID
- Chan, David C.
- Venue
- Annual Review of Pathology: Mechanisms of Disease
- Publisher
- Annual Reviews
- Published
- 2020-01-24
- Volume
- 15
- Issue
- 1
- Pages
- 235-259
- ISSN
- 1553-4006 (ISSN-L)
- 1553-4014
- OpenAlex
- W2978810474
- Cited by
- 1,416
- References
- 150
- Citations by year
- 2026: 191 · 2025: 291 · 2024: 292 · 2023: 228 · 2022: 219 · 2021: 151 · 2020: 43 · 2019: 1
- FWCI
- 9.11
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Annual Review of Pathology Mechanisms of Disease (publishedVersion)
- PubMed (publishedVersion)
- CaltechAUTHORS (California Institute of Technology) (submittedVersion)
- Funders
- National Institute of General Medical Sciences (R35GM127147)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- mitochondrial dynamics, mitochondrial fusion, mitochondrial fission, mitochondrial degradation, dynamin-related proteins, GTPase, mitochondrial morphology, mitochondrial inheritance, mitochondrial DNA maintenance, oxidative phosphorylation, neurodegenerative diseases, cancer, mitochondrial disease
- MeSH terms
- Animals, Disease, DNA, Mitochondrial, Humans, Mitochondria, Neurodegenerative Diseases, Mitochondrial Diseases, Mitochondrial Dynamics
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