ArticleNature communications2016
Tenascin-C drives persistence of organ fibrosis.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 179 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
179 citing papers in PubMed, 1 synthesis or guideline pooled it, 282 citations in OpenAlex.
- Identification of Hub Genes in Idiopathic Pulmonary Fibrosis and Their Association with Lung Cancer by Bioinformatics Analysis.Advances in respiratory medicine · 2023Pooled it
- A bioengineered living cell construct activates metallothionein/zinc/MMP8 and inhibits TGFβ to stimulate remodeling of fibrotic venous leg ulcers.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society · 2020Trial
- New approach methodologies: drug screening platform to identify antifibrotic compounds.Nature protocols · 2026Review
- Transcriptomic Study of Mechanism Driving Conjunctival Fibrosis Following Glaucoma Filtration Surgery.Biomedicines · 2026Article
- Article
- CD248 acts as a mechanosensory switch in fibroblast subsets to establish distinct pathological niches in renal fibrosis.Nature communications · 2026Article
- Epidermal PPARγ Signaling as a Suppressor of Toll-like Receptor-Mediated Inflammation and Fibrosis: Relevance to Cutaneous Squamous Cell Carcinoma.International journal of molecular sciences · 2026Article
- Cellular and molecular regulation of fibrotic postoperative abdominal adhesions.American journal of physiology. Cell physiology · 2026Review
- Hyaluronic acid and tissue mechanics orchestrate mammalian digit tip regeneration.Science (New York, N.Y.) · 2026Article
- Single nuclei/cell transcriptomics reveal DMD driven cell dynamics and mechanisms of fibroblast inflammatory tissue priming in human dystrophic muscle.Research square · 2026Article
- Tissue-layer-resolved proteome landscape of Crohn's disease strictures highlights potential drivers of fibrosis progression.JCI insight · 2026Article
- Mechanical gating of tendon fibrogenic transcription in systemic sclerosis.Nature communications · 2026Article
- Crosstalk between macrophages and fibroblasts contributes to inflammation and damage in giant cell arteritis.Rheumatology (Oxford, England) · 2026Article
- A role for ETV1 and endothelial cell-derived extracellular vesicle microRNAs in priming fibroblast response to vesicle-bound FGF2.bioRxiv : the preprint server for biology · 2026Article
- Versican expression from lung fibroblasts suppresses pulmonary fibrosis.Nature communications · 2026Article
- Combined antagonism of Oncostatin M (OSM) and Interleukin 6 (IL-6) provides both anti-fibrotic and anti-inflammatory benefit in pulmonary fibrosis.bioRxiv : the preprint server for biology · 2026Article
- Composition and Influence of Fibrogenic Niche in Myocardial Fibrosis.Reviews in cardiovascular medicine · 2026Review
- Article
- Unveiling the dental cellular landscape: A comprehensive review of single-cell RNA sequencing in human dental tissues.The Japanese dental science review · 2025Review
- Epigenetic dysregulation in aged muscle stem cells drives mesenchymal progenitor expansion via IL-6 and Spp1 signaling.Nature aging · 2025Article
119 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
Abstract
The factors responsible for maintaining persistent organ fibrosis in systemic sclerosis (SSc) are not known but emerging evidence implicates toll-like receptors (TLRs) in the pathogenesis of SSc. Here we show the expression, mechanism of action and pathogenic role of endogenous TLR activators in skin from patients with SSc, skin fibroblasts, and in mouse models of organ fibrosis. Levels of tenascin-C are elevated in SSc skin biopsy samples, and serum and SSc fibroblasts, and in fibrotic skin tissues from mice. Exogenous tenascin-C stimulates collagen gene expression and myofibroblast transformation via TLR4 signalling. Mice lacking tenascin-C show attenuation of skin and lung fibrosis, and accelerated fibrosis resolution. These results identify tenascin-C as an endogenous danger signal that is upregulated in SSc and drives TLR4-dependent fibroblast activation, and by its persistence impedes fibrosis resolution. Disrupting this fibrosis amplification loop might be a viable strategy for the treatment of SSc.
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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.