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 (637 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
Fusion of somatic cells in vitro or in vivo, which results in somatic cell hybridization.
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: Cell Fusions; Fusion, Cell; Fusions, Cell.
Where it fits in the MeSH classification
- Broader topics
- Cytological Techniques; Cell Physiological Phenomena
- See also
- Hybrid Cells
Research landscape
PubMed indexes 9,728 records tagged with the MeSH heading “Cell Fusion” (counts retrieved 2026-10-29). 533 of them (5.5%) were published from 2020 onward, and the busiest period so far is through 1999 with 5,839 records.
Reviews account for 881 records (9.1%) and meta-analyses for 0. Randomized controlled trials number 1 (0.0%) 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 | 5,839 |
| 2000-2009 | 1,947 |
| 2010-2019 | 1,409 |
| 2020 onward | 533 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 881 | 9.1% |
| Meta-analyses | 0 | 0.0% |
| Randomized controlled trials | 1 | 0.0% |
Method: PubMed query "Cell Fusion"[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 |
|---|---|---|---|---|
| Furin cleavage of SARS-CoV-2 Spike promotes but is not essential for infection and cell-cell fusion | 2021 | Research article Design not recorded in structured metadata | 308 | cc by PMID 33493182 · DOI · PMC7861537 |
| Myomerger induces fusion of non-fusogenic cells and is required for skeletal muscle development | 2017 | Research article Design not recorded in structured metadata | 224 | cc by PMID 28569755 · DOI · PMC5461499 |
| Transplanted photoreceptor precursors transfer proteins to host photoreceptors by a mechanism of cytoplasmic fusion | 2016 | Research article Design not recorded in structured metadata | 181 | cc by PMID 27901042 · DOI · PMC5141374 |
| Cell surface crowding is a tunable energetic barrier to cell-cell fusion | 2025 | Research article Design not recorded in structured metadata | 4 | cc by PMID 40759642 · DOI · PMC12322221 |
Furin cleavage of SARS-CoV-2 Spike promotes but is not essential for infection and cell-cell fusion [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Severe Acute Respiratory Syndrome coronavirus 2 (SARS-CoV-2) infects cells by binding to the host cell receptor ACE2 and undergoing virus-host membrane fusion.
- Closing excerpt
- Our results show that while furin promotes both SARS-CoV-2 infectivity and cell-cell spread it is not essential, suggesting furin inhibitors may reduce but not abolish viral spread.
- 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 (184 words)
Severe Acute Respiratory Syndrome coronavirus 2 (SARS-CoV-2) infects cells by binding to the host cell receptor ACE2 and undergoing virus-host membrane fusion. Fusion is triggered by the protease TMPRSS2, which processes the viral Spike (S) protein to reveal the fusion peptide. SARS-CoV-2 has evolved a multibasic site at the S1-S2 boundary, which is thought to be cleaved by furin in order to prime S protein for TMPRSS2 processing. Here we show that CRISPR-Cas9 knockout of furin reduces, but does not prevent, the production of infectious SARS-CoV-2 virus. Comparing S processing in furin knockout cells to multibasic site mutants reveals that while loss of furin substantially reduces S1-S2 cleavage it does not prevent it. SARS-CoV-2 S protein also mediates cell-cell fusion, potentially allowing virus to spread virion-independently. We show that loss of furin in either donor or acceptor cells reduces, but does not prevent, TMPRSS2-dependent cell-cell fusion, unlike mutation of the multibasic site that completely prevents syncytia formation. Our results show that while furin promotes both SARS-CoV-2 infectivity and cell-cell spread it is not essential, suggesting furin inhibitors may reduce but not abolish viral spread.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 33493182 · DOI · PMC7861537
Myomerger induces fusion of non-fusogenic cells and is required for skeletal muscle development [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Despite the importance of cell fusion for mammalian development and physiology, the factors critical for this process remain to be fully defined, which has severely limited our ability to reconstitute cell fusion.
- Closing excerpt
- Our findings identify myomerger as a fundamental myoblast fusion protein and establish a system that begins to reconstitute mammalian cell fusion.
- 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 (149 words)
Despite the importance of cell fusion for mammalian development and physiology, the factors critical for this process remain to be fully defined, which has severely limited our ability to reconstitute cell fusion. Myomaker (Tmem8c) is a muscle-specific protein required for myoblast fusion. Expression of myomaker in fibroblasts drives their fusion with myoblasts, but not with other myomaker-expressing fibroblasts, highlighting the requirement of additional myoblast-derived factors for fusion. Here we show that Gm7325, which we name myomerger, induces the fusion of myomaker-expressing fibroblasts. Thus, myomaker and myomerger together confer fusogenic activity to otherwise non-fusogenic cells. Myomerger is skeletal muscle-specific and genetic deletion in mice results in a paucity of muscle fibres demonstrating its requirement for normal muscle formation. Myomerger deficient myocytes differentiate and harbour organized sarcomeres but are fusion-incompetent. Our findings identify myomerger as a fundamental myoblast fusion protein and establish a system that begins to reconstitute mammalian cell fusion.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 28569755 · DOI · PMC5461499
Transplanted photoreceptor precursors transfer proteins to host photoreceptors by a mechanism of cytoplasmic fusion [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Photoreceptor transplantation is a potential future treatment for blindness caused by retinal degeneration.
- Closing excerpt
- Understanding this novel mechanism may provide alternate therapeutic strategies at earlier stages of retinal degeneration.
- 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)
Photoreceptor transplantation is a potential future treatment for blindness caused by retinal degeneration. Photoreceptor transplantation restores visual responses in end-stage retinal degeneration, but has also been assessed in non-degenerate retinas. In the latter scenario, subretinal transplantation places donor cells beneath an intact host outer nuclear layer (ONL) containing host photoreceptors. Here we show that host cells are labelled with the donor marker through cytoplasmic transfer-94±4.1% of apparently well-integrated donor cells containing both donor and host markers. We detect the occurrence of Cre-Lox recombination between donor and host photoreceptors, and we confirm the findings through FISH analysis of X and Y chromosomes in sex-discordant transplants. We do not find evidence of nuclear fusion of donor and host cells. The artefactual appearance of integrated donor cells in host retinas following transplantation is most commonly due to material transfer from donor cells. Understanding this novel mechanism may provide alternate therapeutic strategies at earlier stages of retinal degeneration.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 27901042 · DOI · PMC5141374
Cell surface crowding is a tunable energetic barrier to cell-cell fusion [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Cell-cell fusion is fundamental to processes such as muscle formation and viral infection.
- Closing excerpt
- In this work, we show that cell surface crowding presents an underappreciated biophysical barrier that may be tuned developmentally and could be targeted externally to control tissue-specific cell-cell fusion.
- 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 (150 words)
Cell-cell fusion is fundamental to processes such as muscle formation and viral infection. An essential step in fusion is close membrane apposition, but cell membranes are crowded with proteins, glycoproteins, and glycolipids, which must be cleared before a fusion pore can be nucleated. Here, we find that cell surface crowding reduces fusogenicity independent of how fusion is driven. We estimate that crowding presents an energetic barrier to membrane apposition on the scale of ~ 100kBT , greater than that of bare membrane fusion alone. We show that increasing cell surface crowding reduces fusion efficiency of PEG-mediated and fusogen-mediated cell-cell fusion, as well as synthetic membranes under force. Interestingly, we find that differentiating myoblasts naturally decrease their surface crowding prior to fusion. In this work, we show that cell surface crowding presents an underappreciated biophysical barrier that may be tuned developmentally and could be targeted externally to control tissue-specific cell-cell fusion.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40759642 · DOI · PMC12322221
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 Myoblast fusion: lessons from flies and mice [5]
- Research article Electric field-mediated fusion and related electrical phenomena [6]
- Research article Membrane fusion [7]
- Research article Electric field-induced cell-to-cell fusion [8]
- Research article Arbidol: a broad-spectrum antiviral compound that blocks viral fusion [9]
- Research article Biological implications of cell fusion [10]
References
- Papa G, Mallery DL, Albecka A, Welch LG, Cattin-Ortolá J, Luptak J, et al.. Furin cleavage of SARS-CoV-2 Spike promotes but is not essential for infection and cell-cell fusion. . 2021. PMID 33493182 · DOI · PMC7861537
- Quinn ME, Goh Q, Kurosaka M, Gamage DG, Petrany MJ, Prasad V, et al.. Myomerger induces fusion of non-fusogenic cells and is required for skeletal muscle development. . 2017. PMID 28569755 · DOI · PMC5461499
- Singh MS, Balmer J, Barnard AR, Aslam SA, Moralli D, Green CM, et al.. Transplanted photoreceptor precursors transfer proteins to host photoreceptors by a mechanism of cytoplasmic fusion. . 2016. PMID 27901042 · DOI · PMC5141374
- Lee DSW, Oster LF, Son S, Fletcher DA. Cell surface crowding is a tunable energetic barrier to cell-cell fusion. . 2025. PMID 40759642 · DOI · PMC12322221
- Abmayr SM, Pavlath GK. Myoblast fusion: lessons from flies and mice. Development. 2012. PMID 22274696 · DOI · PMC3265056
- Zimmermann U. Electric field-mediated fusion and related electrical phenomena. Biochim Biophys Acta. 1982. PMID 6758848 · DOI
- Poste G, Allison AC. Membrane fusion. Biochim Biophys Acta. 1973. PMID 4360422 · DOI
- Zimmermann U, Vienken J. Electric field-induced cell-to-cell fusion. J Membr Biol. 1982. PMID 7050391 · DOI
- Boriskin YS, Leneva IA, Pécheur EI, Polyak SJ. Arbidol: a broad-spectrum antiviral compound that blocks viral fusion. Curr Med Chem. 2008. PMID 18393857 · DOI
- Ogle BM, Cascalho M, Platt JL. Biological implications of cell fusion. Nat Rev Mol Cell Biol. 2005. PMID 15957005 · DOI
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.
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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.