Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (596 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
The continuous remodeling of mitochondria shape by fission and fusion in response to physiological conditions.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Dynamic, Mitochondrial; Dynamics, Mitochondrial; Mitochondrial Dynamic; Mitochondrial Fusion and Fission; Mitochondrial Fission and Fusion; Mitochondrial Fusion; Fusion, Mitochondrial; Fusions, Mitochondrial.
Where it fits in the MeSH classification
- Broader topics
- Mitochondrial Turnover
Related concepts
- Mitochondria
Research landscape
PubMed indexes 5,549 records tagged with the MeSH heading “Mitochondrial Dynamics” (counts retrieved 2026-10-29). 3,497 of them (63.0%) were published from 2020 onward, and the busiest period so far is 2020 onward with 3,497 records.
Reviews account for 1,095 records (19.7%) and meta-analyses for 0. Randomized controlled trials number 5 (0.1%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 0 |
| 2000-2009 | 0 |
| 2010-2019 | 2,111 |
| 2020 onward | 3,497 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 1,095 | 19.7% |
| Meta-analyses | 0 | 0.0% |
| Randomized controlled trials | 5 | 0.1% |
Method: PubMed query "Mitochondrial Dynamics"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in molecular biology
Molecular biology establishes mechanisms through controlled experiments, often in simplified systems such as purified proteins, cultured cells or model organisms. Such work can show what is possible in a defined system, but whether a pathway matters in a whole organism or in human disease needs further evidence. Check the experimental system, whether findings were reproduced by independent groups, and whether the authors tested the mechanism directly or inferred it from correlation.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| The Balance of MFN2 and OPA1 in Mitochondrial Dynamics, Cellular Homeostasis, and Disease | 2025 | Review article Design not recorded in structured metadata | 86 | cc by PMID 40149969 · DOI · PMC11940761 |
| Molecular mechanisms of mitochondrial quality control | 2025 | Review article Design not recorded in structured metadata | 42 | cc by PMID 40887660 · DOI · PMC12400733 |
| Mitochondrial mechanotransduction through MIEF1 coordinates the nuclear response to forces | 2024 | Research article Design not recorded in structured metadata | 41 | cc by PMID 39433949 · DOI · PMC11628398 |
| Mitochondrial dynamics and their role in the pathogenesis of age-related macular degeneration: A comprehensive review | 2026 | Review article Design not recorded in structured metadata | 10 | cc by PMID 41935442 · DOI · PMC13089171 |
The Balance of MFN2 and OPA1 in Mitochondrial Dynamics, Cellular Homeostasis, and Disease [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Mitochondrial dynamics, governed by fusion and fission, are crucial for maintaining cellular homeostasis, energy production, and stress adaptation.
- Closing excerpt
- Finally, we highlight emerging therapeutic strategies to restore mitochondrial integrity, including mTOR modulation and autophagy-targeted approaches, with potential implications for neurodegenerative disorders.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (142 words)
Mitochondrial dynamics, governed by fusion and fission, are crucial for maintaining cellular homeostasis, energy production, and stress adaptation. MFN2 and OPA1, key regulators of mitochondrial fusion, play essential roles beyond their structural functions, influencing bioenergetics, intracellular signaling, and quality control mechanisms such as mitophagy. Disruptions in these processes, often caused by MFN2 or OPA1 mutations, are linked to neurodegenerative diseases like Charcot-Marie-Tooth disease type 2A (CMT2A) and autosomal dominant optic atrophy (ADOA). This review explores the molecular mechanisms underlying mitochondrial fusion, the impact of MFN2 and OPA1 dysfunction on oxidative phosphorylation and autophagy, and their role in disease progression. Additionally, we discuss the divergent cellular responses to MFN2 and OPA1 mutations, particularly in terms of proliferation, senescence, and metabolic signaling. Finally, we highlight emerging therapeutic strategies to restore mitochondrial integrity, including mTOR modulation and autophagy-targeted approaches, with potential implications for neurodegenerative disorders.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40149969 · DOI · PMC11940761
Molecular mechanisms of mitochondrial quality control [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Mitochondria produce adenosine triphosphate (ATP), the main source of cellular energy.
- Closing excerpt
- In this review, we discuss various ways by which the MQC system maintains mitochondrial homeostasis, highlight the relationships between these pathways, and characterize the life cycle of individual mitochondria under the MQC system.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (99 words)
Mitochondria produce adenosine triphosphate (ATP), the main source of cellular energy. To maintain normal function, cells rely on a complex mitochondrial quality control (MQC) system that regulates mitochondrial homeostasis, including mitochondrial dynamics, mitochondrial dynamic localization, mitochondrial biogenesis, clearance of damaged mitochondria, oxygen radical scavenging, and mitochondrial protein quality control. The MQC system also involves coordination of other organelles, such as the endoplasmic reticulum, lysosomes, and peroxisomes. In this review, we discuss various ways by which the MQC system maintains mitochondrial homeostasis, highlight the relationships between these pathways, and characterize the life cycle of individual mitochondria under the MQC system.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40887660 · DOI · PMC12400733
Mitochondrial mechanotransduction through MIEF1 coordinates the nuclear response to forces [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Tissue-scale architecture and mechanical properties instruct cell behaviour under physiological and diseased conditions, but our understanding of the underlying mechanisms remains fragmentary.
- Closing excerpt
- We propose that mitochondria fulfil a unifying signalling function by which the mechanical tissue microenvironment coordinates complementary cell functions.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (154 words)
Tissue-scale architecture and mechanical properties instruct cell behaviour under physiological and diseased conditions, but our understanding of the underlying mechanisms remains fragmentary. Here we show that extracellular matrix stiffness, spatial confinements and applied forces, including stretching of mouse skin, regulate mitochondrial dynamics. Actomyosin tension promotes the phosphorylation of mitochondrial elongation factor 1 (MIEF1), limiting the recruitment of dynamin-related protein 1 (DRP1) at mitochondria, as well as peri-mitochondrial F-actin formation and mitochondrial fission. Strikingly, mitochondrial fission is also a general mechanotransduction mechanism. Indeed, we found that DRP1- and MIEF1/2-dependent fission is required and sufficient to regulate three transcription factors of broad relevance-YAP/TAZ, SREBP1/2 and NRF2-to control cell proliferation, lipogenesis, antioxidant metabolism, chemotherapy resistance and adipocyte differentiation in response to mechanical cues. This extends to the mouse liver, where DRP1 regulates hepatocyte proliferation and identity-hallmark YAP-dependent phenotypes. We propose that mitochondria fulfil a unifying signalling function by which the mechanical tissue microenvironment coordinates complementary cell functions.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39433949 · DOI · PMC11628398
Mitochondrial dynamics and their role in the pathogenesis of age-related macular degeneration: A comprehensive review [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Age-related macular degeneration (AMD) is a leading cause of irreversible blindness in the elderly and has a multifactorial etiology involving advanced age, genetic susceptibility, and environmental risk factors.
- Closing excerpt
- As the field advances, the integration of biomarker development and personalized approaches holds the potential to transform the clinical landscape of AMD by addressing the root causes of cellular dysfunction.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (201 words)
Age-related macular degeneration (AMD) is a leading cause of irreversible blindness in the elderly and has a multifactorial etiology involving advanced age, genetic susceptibility, and environmental risk factors. Accumulating evidence suggests that mitochondrial dysfunction is a central pathogenic mechanism in AMD, particularly in the retinal pigment epithelium (RPE). The RPE is critical for retinal homeostasis, and its high metabolic activity renders it vulnerable to age-related mitochondrial dysfunction. In AMD, the core processes of mitochondrial dynamics-fission, fusion, biogenesis, and mitophagy-are profoundly dysregulated, leading to a fragmented and dysfunctional mitochondrial network. This failure of quality control results in bioenergetic deficits, excessive oxidative stress, and the release of damage-associated molecular patterns that fuel chronic inflammation and complement-mediated damage. Experimental models and human tissue studies have strengthened the link between mitochondrial dysfunction and AMD pathology, revealing structural abnormalities, mitochondrial DNA (mtDNA) damage, and altered metabolic signatures. Therapeutic strategies targeting mitochondrial pathways, including mitochondria-targeted antioxidants, dynamic modulators, and enhancers of biogenesis and mitophagy, such as agents that restore defective mitophagosome formation, represent promising avenues for intervention. As the field advances, the integration of biomarker development and personalized approaches holds the potential to transform the clinical landscape of AMD by addressing the root causes of cellular dysfunction.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41935442 · DOI · PMC13089171
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article The cell biology of mitochondrial membrane dynamics [5]
- Research article Mitochondrial Dynamics and Its Involvement in Disease [6]
- Research article Mitochondrial dynamics: overview of molecular mechanisms [7]
- Research article Mitochondrial Dynamics and Metabolic Regulation [8]
- Research article Mitochondrial dynamics in health and disease: mechanisms and potential targets [9]
- Research article Metabolic regulation of mitochondrial dynamics [10]
References
- Zanfardino P, Amati A, Perrone M, Petruzzella V. The Balance of MFN2 and OPA1 in Mitochondrial Dynamics, Cellular Homeostasis, and Disease. . 2025. PMID 40149969 · DOI · PMC11940761
- Li W, Gui Y, Guo C, Huang Y, Liu Y, Yu X, et al.. Molecular mechanisms of mitochondrial quality control. . 2025. PMID 40887660 · DOI · PMC12400733
- Romani P, Benedetti G, Cusan M, Arboit M, Cirillo C, Wu X, et al.. Mitochondrial mechanotransduction through MIEF1 coordinates the nuclear response to forces. . 2024. PMID 39433949 · DOI · PMC11628398
- Chen KY, Chan HC, Lin WW, Chan CM. Mitochondrial dynamics and their role in the pathogenesis of age-related macular degeneration: A comprehensive review. . 2026. PMID 41935442 · DOI · PMC13089171
- Giacomello M, Pyakurel A, Glytsou C, Scorrano L. The cell biology of mitochondrial membrane dynamics. Nat Rev Mol Cell Biol. 2020. PMID 32071438 · DOI
- Chan DC. Mitochondrial Dynamics and Its Involvement in Disease. Annu Rev Pathol. 2020. PMID 31585519 · DOI
- Tilokani L, Nagashima S, Paupe V, Prudent J. Mitochondrial dynamics: overview of molecular mechanisms. Essays Biochem. 2018. PMID 30030364 · DOI · PMC6056715
- Wai T, Langer T. Mitochondrial Dynamics and Metabolic Regulation. Trends Endocrinol Metab. 2016. PMID 26754340 · DOI
- Chen W, Zhao H, Li Y. Mitochondrial dynamics in health and disease: mechanisms and potential targets. Signal Transduct Target Ther. 2023. PMID 37669960 · DOI · PMC10480456
- Mishra P, Chan DC. Metabolic regulation of mitochondrial dynamics. J Cell Biol. 2016. PMID 26858267 · DOI · PMC4754720
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
See how EvidenceLib is built. Spotted an error? Email support@evidencehelix.com.
Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.