ArticlePloS one2015
Fn14, a Downstream Target of the TGF-β Signaling Pathway, Regulates Fibroblast Activation.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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.
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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
17 citing papers in PubMed, 25 citations in OpenAlex.
- Single-cell transcriptome reveals keratinocyte subclusters contributing to altered differentiation and inflammatory responses in atopic dermatitis.Nature communications · 2026Article
- Research progress on TWEAK/Fn14 signaling in chronic wound healing.Frontiers in surgery · 2026Review
- CagA-dependent expression of anti-inflammatory cytokine IL-13 and TNFRSF member Fn14 inFrontiers in microbiology · 2026Article
- Comparative effectiveness of plant-derived compounds in keloid management: a review.Frontiers in pharmacology · 2025Review
- Extracellular Vesicle-Associated TWEAK Contributes to Vascular Inflammation and Remodeling During Acute Cellular Rejection.JACC. Basic to translational science · 2023Article
- Distal Lung Microenvironment Triggers Release of Mediators Recognized as Potential Systemic Biomarkers for Idiopathic Pulmonary Fibrosis.International journal of molecular sciences · 2021Article
- Article
- Interruption of neutrophil extracellular traps formation dictates host defense and tubular HOXA5 stability to augment efficacy of anti-Fn14 therapy against septic AKI.Theranostics · 2021Article
- Smad‑binding decoy reduces extracellular matrix expression in human hypertrophic scar fibroblasts.Molecular medicine reports · 2020Article
- Defining the Cardiac Fibroblast Secretome in a Fibrotic Microenvironment.Journal of the American Heart Association · 2020Article
- Hypoxia-Induced Epithelial-To-Mesenchymal Transition Mediates Fibroblast Abnormalities via ERK Activation in Cutaneous Wound Healing.International journal of molecular sciences · 2019Article
- Fn14 deficiency ameliorates psoriasis-like skin disease in a murine model.Cell death & disease · 2018Article
- Aberrant expression of miR-663 and transforming growth factor-β1 in nasal polyposis in children.Experimental and therapeutic medicine · 2018Article
- Topical TWEAK Accelerates Healing of Experimental Burn Wounds in Mice.Frontiers in pharmacology · 2018Article
- Ginsenoside Rb1 improves cardiac function and remodeling in heart failure.Experimental animals · 2017Article
- Role of miR-24, Furin, and Transforming Growth Factor-β1 Signal Pathway in Fibrosis After Cardiac Infarction.Medical science monitor : international medical journal of experimental and clinical research · 2017Article
- TWEAK/Fn14 Activation Participates in Skin Inflammation.Mediators of inflammation · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibrosis, the hallmark of human injuries and diseases such as serious burns, is characterized by excessive collagen synthesis and myofibroblast accumulation. Transforming growth factor-β (TGF-β), a potent inducer of collagen synthesis, has been implicated in fibrosis in animals. In addition to TGF-β, fibroblast growth factor-inducible molecule 14 (Fn14) has been reported to play an important role in fibrotic diseases, such as cardiac fibrosis. However, the function and detailed regulatory mechanism of Fn14 in fibrosis are unclear. Here, we investigated the effect of Fn14 on the activation of human dermal fibroblasts. In normal dermal fibroblasts, TGF-β signaling increased collagen production and Fn14 expression. Furthermore, Fn14 siRNA blocked extracellular matrix gene expression; even when TGF-β signaling was activated by TGF-β1, fibroblast activation remained blocked in the presence of Fn14 siRNA. Overexpressing Fn14 increased extracellular matrix gene expression. In determining the molecular regulatory mechanism, we discovered that SMAD4, an important TGF-β signaling co-mediator, bound to the Fn14 promoter and activated Fn14 transcription. Taken together, these results indicate that the TGF-β signaling pathway activates Fn14 expression through the transcription factor SMAD4 and that activated Fn14 expression increases extracellular matrix synthesis and fibroblast activation. Therefore, Fn14 may represent a promising approach to preventing the excessive accumulation of collagen or ECM in skin fibrosis.
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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.