ArticleThe EMBO journal2006
TWEAK, via its receptor Fn14, is a novel regulator of mesenchymal progenitor cells and skeletal muscle regeneration.
Article in The EMBO journal, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
113 citing papers in PubMed, 1 synthesis or guideline pooled it, 215 citations in OpenAlex.
- A potential fate decision landscape of the TWEAK/Fn14 axis on stem and progenitor cells: a systematic review.Stem cell research & therapy · 2022Pooled it
- Human skeletal muscle macrophages increase following cycle training and are associated with adaptations that may facilitate growth.Scientific reports · 2019Trial
- Muscle Fn14 gene expression is associated with fat-free mass retention during energy deficit at high altitude.Physiological reports · 2018Trial
- TWEAK-induced alternative NF-κB signaling regulates Cxcl10 and Mymx to promote myoblast-to-myotube fusion and muscle regeneration.Communications biology · 2026Article
- Fn14 is an activity-dependent, Bmal1-regulated cytokine receptor that induces rod-like microglia and restricts neuronal activity in vivo.Cell reports · 2026Article
- Inhibition of TWEAK/Fn14 Ameliorates Sarcopenic Obesity by Restoring Mitochondrial Biogenesis via the AMPK/SIRT1/PGC-1α Axis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Article
- Multi-Omics Identification ofBiology · 2025Article
- Article
- Unraveling the bidirectional relationship between muscle inflammation and satellite cells activity: influencing factors and insights.Journal of muscle research and cell motility · 2025Review
- Fibroblast growth factor-inducible 14 regulates satellite cell self-renewal and expansion during skeletal muscle repair.JCI insight · 2025Article
- Fibroblast growth factor-inducible 14 regulates satellite cell self-renewal and expansion during skeletal muscle repair.bioRxiv : the preprint server for biology · 2025Article
- Article
- Cytokine expression and cytokine-mediated cell-cell communication during skeletal muscle regeneration revealed by integrative analysis of single-cell RNA sequencing data.Journal of cell communication and signaling · 2024Article
- TWEAK/Fn14 signalling driven super-enhancer reprogramming promotes pro-metastatic metabolic rewiring in triple-negative breast cancer.Nature communications · 2024Article
- Review
- The cytokine receptor Fn14 is a molecular brake on neuronal activity that mediates circadian functionbioRxiv : the preprint server for biology · 2024Article
- Fn14 promotes myoblast fusion during regenerative myogenesis.Life science alliance · 2023Article
- Leveraging single-cell RNA sequencing to unravel the impact of aging on stroke recovery mechanisms in mice.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Platelet-derived chemokines promote skeletal muscle regeneration by guiding neutrophil recruitment to injured muscles.Nature communications · 2023Article
- Article
53 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 6 institutions in 3 countries.
Funding
Abstract
Inflammation participates in tissue repair through multiple mechanisms including directly regulating the cell fate of resident progenitor cells critical for successful regeneration. Upon surveying target cell types of the TNF ligand TWEAK, we observed that TWEAK binds to all progenitor cells of the mesenchymal lineage and induces NF-kappaB activation and the expression of pro-survival, pro-proliferative and homing receptor genes in the mesenchymal stem cells, suggesting that this pro-inflammatory cytokine may play an important role in controlling progenitor cell biology. We explored this potential using both the established C2C12 cell line and primary mouse muscle myoblasts, and demonstrated that TWEAK promoted their proliferation and inhibited their terminal differentiation. By generating mice deficient in the TWEAK receptor Fn14, we further showed that Fn14-deficient primary myoblasts displayed significantly reduced proliferative capacity and altered myotube formation. Following cardiotoxin injection, a known trigger for satellite cell-driven skeletal muscle regeneration, Fn14-deficient mice exhibited reduced inflammatory response and delayed muscle fiber regeneration compared with wild-type mice. These results indicate that the TWEAK/Fn14 pathway is a novel regulator of skeletal muscle precursor cells and illustrate an important mechanism by which inflammatory cytokines influence tissue regeneration and repair. Coupled with our recent demonstration that TWEAK potentiates liver progenitor cell proliferation, the expression of Fn14 on all mesenchymal lineage progenitor cells supports a broad involvement of this pathway in other tissue injury and disease settings.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.