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Drp1-Dependent Mitochondrial Fission Plays Critical Roles in Physiological and Pathological Progresses in Mammals
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Current research has demonstrated that mitochondrial morphology, distribution, and function are maintained by the balanced regulation of mitochondrial fission and fusion, and perturbation of the homeostasis between these processes has been related to cell or organ dysfunction and abnormal mitochondrial redistribution. Abnormal mitochondrial fusion induces the fragmentation of mitochondria from a tubular morphology into pieces; in contrast, perturbed mitochondrial fission results in the fusion of adjacent mitochondria. A member of the dynamin family of large GTPases, dynamin-related protein 1 (Drp1), effectively influences cell survival and apoptosis by mediating the mitochondrial fission process in mammals. Drp1-dependent mitochondrial fission is an intricate process regulating both cellular and organ dynamics, including development, apoptosis, acute organ injury, and various diseases. Only after clarification of the regulative mechanisms of this critical protein in vivo and in vitro will it set a milestone for preventing mitochondrial fission related pathological processes and refractory diseases.
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“Mitochondrial fission-fusion dynamics through alterations of Drp1, Parkin, and Pink1 functions (23,24), which play essential roles in mitophagy induction and mitochondrial quality control during healthy brain aging, are disrupted in various neurodegenerative diseases, including Parkinson’s disease (PD) and AD (25).”
From Alzheimer's Disease–Associated Amyloid-β Precursor Protein Prevents Aging Stress–Induced Mitophagy and Fumarate Depletion to Improve Antitumor Immunity (2025) · cites this paper as [25]
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Metadata
- Authors
- Hu, C., Huang, Y., & Li, L.
- Affiliations
- First Affiliated Hospital Zhejiang University (CN)
- Corresponding author
- Li, Lanjuan
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2017-01-13
- Volume
- 18
- Issue
- 1
- Pages
- 144
- ISSN
- 1422-0067 (ISSN-L)
- PMC
- PMC5297777
- OpenAlex
- W2573555074
- Cited by
- 302
- References
- 144
- Citations by year
- 2026: 27 · 2025: 34 · 2024: 33 · 2023: 32 · 2022: 29 · 2021: 36 · 2020: 35 · 2019: 27 · 2018: 28 · 2017: 18
- FWCI
- 2.76
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- International Journal of Molecular Sciences (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Natural Science Foundation of China (81471794, 10002004, 81121002)
- Science Fund for Creative Research Groups
- National Science and Technology Major Project (2012ZX10002004)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- Drp1, mitochondrial fission, mitochondrial fusion, mitochondrial morphology, apoptosis, mitochondrial distribution, organ damage, mitochondrial homeostasis, mitochondrial disease
- MeSH terms
- Animals, Disease, Humans, Mammals, Protein Processing, Post-Translational, Apoptosis, Dynamins, Mitochondrial Dynamics
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.
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