Cited by 303Mitochondrial Function and PathologyAutophagy in Disease and TherapyCell death mechanisms and regulation

Drp1-Dependent Mitochondrial Fission Plays Critical Roles in Physiological and Pathological Progresses in Mammals

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Hu, Chenxia, Huang, Yong, Li, Lanjuan·2017·International Journal of Molecular Sciences

Abstract

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 are disrupted in various neurodegenerative diseases, including Parkinson's disease and Alzheimer's disease.

    “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]

    Section 6 (page unavailable) links altered Drp1-dependent mitochondrial dynamics to Parkinson’s and Alzheimer’s diseases and discusses parkin’s effects on neuronal mitochondrial morphology. Its PINK1 discussion concerns ischemic injury, not disruption in those neurodegenerative diseases; the copy does not establish the claimed disease link for all three proteins. (LLM, conf=0.86)

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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)
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 · 2016: 1
FWCI
2.76
Type
journal article
Language
en
Open access
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
  • Health Sciences › Medicine › Epidemiology › 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

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