The DOI matches its Crossref record; 144 of the 144 references it cites were found in a registry or an index.
Drp1-Dependent Mitochondrial Fission Plays Critical Roles in Physiological and Pathological Progresses in Mammals
Open accessAbstract
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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Fission and selective fusion govern mitochondrial segregation and elimination by autophagy
Twig, G., Elorza, A., Molina, A. J. A., Mohamed, H., Wikstrom, J. D., Walzer, G., Stiles, L., Haigh, S. E., Katz, S., Las, G., et al. (2008) · The EMBO Journal · doi:10.1038/sj.emboj.7601963 · Cited by 3,082
Dynamin-related Protein Drp1 Is Required for Mitochondrial Division in Mammalian Cells
Smirnova, E., Griparić, L., Shurland, D., & van der Bliek, A. M. (2001) · Molecular Biology of the Cell · doi:10.1091/mbc.12.8.2245 · Cited by 1,938
During autophagy mitochondria elongate, are spared from degradation and sustain cell viability
Gomes, L. C., Benedetto, G. D., & Scorrano, L. (2011) · Nature Cell Biology · doi:10.1038/ncb2220 · Cited by 1,735
Disruption of Fusion Results in Mitochondrial Heterogeneity and Dysfunction
Chen, H., Chomyn, A., & Chan, D. C. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.m503062200 · Cited by 1,376 · cited 1×
“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 [2,3].”
BackgroundRambold, A. S., Kostelecky, B., Elia, N., & Lippincott‐Schwartz, J. (2011) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1107402108 · Cited by 1,188
Otera, H., Wang, C., Cleland, M. M., Setoguchi, K., Yokota, S., Youle, R. J., & Mihara, K. (2010) · Journal of Cell Biology · doi:10.1083/jcb.201007152 · Cited by 1,110 · cited 1×
“Mff knockdown has been shown to induce mitochondrial elongation in mammalian cells, whereas overexpression of Mff recruits Drp1 for mitochondrial fragmentation [17].”
BackgroundCribbs, J. T., & Strack, S. (2007) · EMBO Reports · doi:10.1038/sj.embor.7401062 · Cited by 1,061
Endoplasmic reticulum-mitochondria contacts: Function of the junction
Rowland, A. A., & Voeltz, G. K. (2012) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm3440 · Cited by 1,018 · cited 1×
“In general, when ER starts to encircle the mitochondria, the mitochondria immediately divide and mitochondrial fission factor (Mff)-dependent Drp1 assembly is subsequently initiated [16].”
BackgroundWang, Z., Jiang, H., Chen, S., Du, F., & Wang, X. (2012) · Cell · doi:10.1016/j.cell.2011.11.030 · Cited by 949
Mańczak, M., Calkins, M. J., & Reddy, P. H. (2011) · Human Molecular Genetics · doi:10.1093/hmg/ddr139 · Cited by 847
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Wang, G., Zhao, Y., Liu, G., Du, Y., Liu, S., Yang, Y., Bu, S., & Zhao, B. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27198451
Ma, J., Zhang, H., Wu, L., Shen, H., Chen, A., Wu, A., & Hu, Y. (2026) · Tissue and Cell · doi:10.1016/j.tice.2026.104001
Fu, Z.-B., Li, Y., Ding, S.-Y., Luo, J.-Y., Ma, X., & Yu, Z.-X. (2026) · Tissue and Cell · doi:10.1016/j.tice.2026.104089
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
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