ReviewFrontiers in medicine2015
Signaling in Fibrosis: TGF-β, WNT, and YAP/TAZ Converge.
Review in Frontiers in medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 291 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
291 citing papers in PubMed, 1 synthesis or guideline pooled it, 418 citations in OpenAlex.
- A genome-wide association meta-analysis implicates Hedgehog and Notch signaling in Dupuytren's disease.Nature communications · 2024Pooled it
- Comparison of two antifibrotic treatments for lung fibrosis in post-COVID-19 syndrome: A randomized, prospective study.Medicina clinica · 2023Trial
- E3 Ubiquitin Ligases in MASH-Associated Liver Fibrosis: Mechanisms and Therapeutic Opportunities.Liver international : official journal of the International Association for the Study of the Liver · 2026Review
- Review
- Cellular crosstalk of fibroblast-myofibroblast transition in intestinal homeostasis and disease.Biomarker research · 2026Review
- The Fibro-Inflammatory Ovary: Stromal Fibrosis, Extracellular Matrix Remodeling, and Mechanotransduction in Female Infertility.Current issues in molecular biology · 2026Review
- A Photothermally Amplified Enzyme-Nitric Oxide Co-Regulatory System Reprograms Pathological ECM-Fibroblast Crosstalk to Alleviate Hypertrophic Scarring.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Sustained YAP/TAZ activation promotes aberrant alveolar epithelial cell differentiation and drives persistent fibrotic remodeling.JCI insight · 2026Article
- Review
- Article
- Aortic carboxypeptidase-like protein potentiates β1 integrin signaling in mesenchymal progenitors.Life science alliance · 2026Article
- Astaxanthin Alleviates Bleomycin-Induced Pulmonary Fibrosis in Mice by Suppressing the Fibroblast-to-Myofibroblast Transition and Collagen Deposition.Molecular nutrition & food research · 2026Article
- Proof-of-Concept Evaluation of Primary Human FAP-CAR-NK Cells Targeting Activated Fibroblasts in Pulmonary Fibrosis.International journal of molecular sciences · 2026Article
- Mechanotransduction and its impact on regenerative medicine in orthopedic rehabilitation (Review).International journal of molecular medicine · 2026Review
- Mechanobiology of the Hippo-YAP Signaling Network.Cold Spring Harbor perspectives in biology · 2026Article
- Fibrotic differentiation profile of skeletal and cardiac muscle fibroadipogenic progenitors in D2-mdx mouse.Journal of neuromuscular diseases · 2026Article
- A Conceptual Fascial Memory Reset Hypothesis: Mechanobiological Insights into Stacking Fascia as an Ultrasound-Visible Structural Phenotype and the Potential Role of Fascial Hydrorelease.International journal of molecular sciences · 2026Article
- Dynamic Organelle Remodeling in HIV-Associated Myocardial Disease: Mechanisms, Fibrotic Pathways, and Therapeutic Opportunities.Current issues in molecular biology · 2026Review
- Review
- WNT3a induces external anal sphincter fibrosis and dysfunction in rabbits.American journal of physiology. Gastrointestinal and liver physiology · 2026Article
231 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
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic organ injury leads to fibrosis and eventually organ failure. Fibrosis is characterized by excessive synthesis, remodeling, and contraction of extracellular matrix produced by myofibroblasts. Myofibroblasts are the key cells in the pathophysiology of fibrotic disorders and their differentiation can be triggered by multiple stimuli. To develop anti-fibrotic therapies, it is of paramount importance to understand the molecular basis of the signaling pathways contributing to the activation and maintenance of myofibroblasts. Several signal transduction pathways, such as transforming growth factor (TGF)-β, Wingless/Int (WNT), and more recently yes-associated protein 1 (YAP)/transcriptional coactivator with PDZ-binding motif (TAZ) signaling, have been linked to the pathophysiology of fibrosis. Activation of the TGF-β1-induced SMAD complex results in the upregulation of genes important for myofibroblast function. Similarly, WNT-stabilized β-catenin translocates to the nucleus and initiates transcription of its target genes. YAP and TAZ are two transcriptional co-activators from the Hippo signaling pathway that also rely on nuclear translocation for their functioning. These three signal transduction pathways have little molecular similarity but do share one principle: the cytosolic/nuclear regulation of its transcriptional activators. Past research on these pathways often focused on the isolated cascades without taking other signaling pathways into account. Recent developments show that parts of these pathways converge into an intricate network that governs the activation and maintenance of the myofibroblast phenotype. In this review, we discuss the current understanding on the signal integration between the TGF-β, WNT, and YAP/TAZ pathways in the development of organ fibrosis. Taking a network-wide view on signal transduction will provide a better understanding on the complex and versatile processes that underlie the pathophysiology of fibrotic disorders.
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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.