Mitochondrial dynamics in health and disease: mechanisms and potential targets
Open accessAbstract
Mitochondria are organelles that are able to adjust and respond to different stressors and metabolic needs within a cell, showcasing their plasticity and dynamic nature. These abilities allow them to effectively coordinate various cellular functions. Mitochondrial dynamics refers to the changing process of fission, fusion, mitophagy and transport, which is crucial for optimal function in signal transduction and metabolism. An imbalance in mitochondrial dynamics can disrupt mitochondrial function, leading to abnormal cellular fate, and a range of diseases, including neurodegenerative disorders, metabolic diseases, cardiovascular diseases and cancers. Herein, we review the mechanism of mitochondrial dynamics, and its impacts on cellular function. We also delve into the changes that occur in mitochondrial dynamics during health and disease, and offer novel perspectives on how to target the modulation of mitochondrial dynamics.
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Switching of a glycolytic fiber to an oxidative IIA type correlates with elongation of mitochondria.
“Furthermore, switching of a glycolytic fiber to an oxidative IIA type correlate with elongation of mitochondria, suggesting a link between mitochondrial fusion and metabolic states [43].”
From Mitochondrial Adaptation in Skeletal Muscle: Impact of Obesity, Caloric Restriction, and Dietary Compounds (2024) · cites this paper as [43]
Knockout models with mtDNA depletion show a progressive decline in exercise performance, accompanied by impaired electron transport chain, particularly for complex I and IV.
“As result of mtDNA depletion, studies with knockout models also show a progressive decline in exercise performance, accompanied by impaired electron transport chain, particularly for complex I and IV [43].”
From Mitochondrial Adaptation in Skeletal Muscle: Impact of Obesity, Caloric Restriction, and Dietary Compounds (2024) · cites this paper as [43]
Oxidative muscle fibers, such as type I and IIA, contain elongated mitochondrial networks with heightened fusion rates dependent on MFN1 and MFN2.
“Oxidative muscle fibers, such as type I and IIA, contain elongated mitochondrial networks with heightened fusion rates that are dependent on MFN1 and MFN2 [43].”
From Mitochondrial Adaptation in Skeletal Muscle: Impact of Obesity, Caloric Restriction, and Dietary Compounds (2024) · cites this paper as [43]
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Titration of mitochondrial fusion rescues <i>Mff</i> -deficient cardiomyopathy
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Mitochondrial dynamics in the central regulation of metabolism
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Flagged first, then by citations
Research works printed but not linked: 1
- [72]Morin M Moindjie H Nahmias C [Mitochondrial transport: How does it impact cancer?] Med. Sci. (Paris) 2022 38 585 593 35766857
Cited by
Sorted by citations
Zhang, J., Zhang, Y., Wang, J., Xia, Y., Zhang, J., & Chen, L. (2024) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-024-01911-3 · Cited by 1,138 · see citing works
“Alterations in the expression levels of proteins related to fi ssion/fusion processes (such as Opa1, Drp1, MFN1/2, Fis1) 298 and post-translational modi fi cations of Drp1 299,300 may bias mitochondria towards excessive fi ssion, increasing mitochondrial fragmentation, leading to damage in…”
BackgroundProtein neddylation and its role in health and diseases
Zhang, S., Yu, Q., Li, Z., Zhao, Y., & Sun, Y. (2024) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-024-01800-9 · Cited by 171 · see citing works
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- Authors
- Chen, W., Zhao, H., & Li, Y.
- Affiliations
- Chongqing University (CN)
- Corresponding author
- Zhao, Huakan
- Li, Yongsheng
- Venue
- Signal Transduction and Targeted Therapy
- Published
- 2023-09-06
- Volume
- 8
- Issue
- 1
- Pages
- 333-333
- ISSN
- 2059-3635 (ISSN-L)
- PMC
- PMC10480456
- OpenAlex
- W4386448978
- Cited by
- 1,306
- References
- 323
- Citations by year
- 2026: 481 · 2025: 560 · 2024: 259 · 2023: 5 · 2016: 1
- FWCI
- 34.28
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Signal Transduction and Targeted Therapy (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Science Foundation of China | Major International Joint Research Programme (81920108027)
- National Natural Science Foundation of China (82273212)
- 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 fission, mitochondrial fusion, mitophagy, mitochondrial transport, mitochondrial plasticity, mitochondrial metabolism, neurodegenerative diseases, metabolic disorders, cardiovascular disease, cancer, therapeutic target
- MeSH terms
- Cardiovascular Diseases, Cell Differentiation, Humans, Mitochondria, Mitochondrial Dynamics, Mitophagy
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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