ArticleNature medicine2015
Nilotinib reduces muscle fibrosis in chronic muscle injury by promoting TNF-mediated apoptosis of fibro/adipogenic progenitors.
Article in Nature medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 472 papers, 1 of them a synthesis that pooled it.
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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
472 citing papers in PubMed, 1 synthesis or guideline pooled it, 697 citations in OpenAlex.
- Skeletal muscle alterations in Marfan syndrome: a systematic review.Journal of muscle research and cell motility · 2025Pooled it
- Pathogenic transcriptional reprogramming of fibro-adipogenic progenitors in mice with FOP and its mitigation by inhibition of ACVR1 and activin A.bioRxiv : the preprint server for biology · 2026Article
- Metabolic Vulnerability and Regenerative Failure of the External Urethral Sphincter: A Ferroptosis-Associated Framework for Stress Urinary Incontinence.Biomolecules · 2026Review
- Integrating and Orchestrating Multiple Components of Skeletal Muscle Injury and Regeneration.American journal of physiology. Cell physiology · 2026Article
- Treating age-related loss of muscle mass and function: Where should we be focusing?The Journal of physiology · 2026Review
- The hallmarks of skeletal muscle health.Nature metabolism · 2026Review
- Phase-transition failure in aged skeletal muscle regeneration.Biogerontology · 2026Review
- State-Dependent FGF Signaling in Satellite Cell-Mediated Skeletal Muscle Regeneration and Pathological Remodeling.Biomolecules · 2026Review
- FAP-derived CCL2 is required for adequate monocyte/macrophage infiltration to support acute skeletal muscle injury repair.iScience · 2026Article
- Epigenetic Skeletal Muscle Memory: The Impact of Physical Activity on Aging and Post-Injury Regeneration.Genes · 2026Review
- Phenotypic divergence in rotator cuff tear and volumetric muscle loss mouse models following fibroadipogenic progenitor depletion.Bone & joint research · 2026Article
- Mesenchymal Stromal Cell-Mediated Intercellular Communication: Mapping the Interactome for Skeletal Muscle Homeostasis and Regeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Macrophage regulation of extracellular matrix remodeling in aging skeletal muscle.Ageing research reviews · 2026Review
- A Multi-Institution Biobanking Pipeline for Primary Human Satellite Cells and Fibro-Adipogenic Progenitors.bioRxiv : the preprint server for biology · 2026Article
- Resident mesenchymal progenitor cells require autocrine IGF-I in homeostatic and regenerating skeletal muscle.Stem cell reports · 2026Article
- Sympathetic nervous system-mediated fibro-adipogenic progenitor mobilization drives stroke-related sarcopenia.Cell discovery · 2026Article
- Systemic regeneration medicines for muscular dystrophy: progress and challenges in pro-regenerative drug development.Cell regeneration (London, England) · 2026Review
- Single cell analysis of muscle contracture in cerebral palsy reveals profibrotic and antimyogenic stem cell populations with altered cell-cell interactions.American journal of physiology. Cell physiology · 2026Article
- Fibroadipogenic progenitor-secreted prostaglandin E2 coordinates stem cell fate via autocrine and paracrine crosstalk in healthy and dystrophic muscle.Cell death and differentiation · 2026Article
- Single-nucleus transcriptomics dissects beef quality variation: coordinated reprogramming of myofiber metabolism, FAPs Fate, and ECM-vascular signaling.BMC genomics · 2026Article
412 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
Abstract
Depending on the inflammatory milieu, injury can result either in a tissue's complete regeneration or in its degeneration and fibrosis, the latter of which could potentially lead to permanent organ failure. Yet how inflammatory cells regulate matrix-producing cells involved in the reparative process is unknown. Here we show that in acutely damaged skeletal muscle, sequential interactions between multipotent mesenchymal progenitors and infiltrating inflammatory cells determine the outcome of the reparative process. We found that infiltrating inflammatory macrophages, through their expression of tumor necrosis factor (TNF), directly induce apoptosis of fibro/adipogenic progenitors (FAPs). In states of chronic damage, however, such as those in mdx mice, macrophages express high levels of transforming growth factor β1 (TGF-β1), which prevents the apoptosis of FAPs and induces their differentiation into matrix-producing cells. Treatment with nilotinib, a kinase inhibitor with proposed anti-fibrotic activity, can block the effect of TGF-β1 and reduce muscle fibrosis in mdx mice. Our findings reveal an unexpected anti-fibrotic role of TNF and suggest that disruption of the precisely timed progression from a TNF-rich to a TGF-β-rich environment favors fibrotic degeneration of the muscle during chronic injury.
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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.