ArticleSignal transduction and targeted therapy2024
TEA domain transcription factor 1(TEAD1) induces cardiac fibroblasts cells remodeling through BRD4/Wnt4 pathway.
Article in Signal transduction and targeted therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 35 citations in OpenAlex.
- Hippo Pathway-YAP/TAZ Signaling: Molecular Mechanisms, Biological Function, Diseases, and Therapeutic Targets.MedComm · 2026Review
- ZEB2 SUMOylation in Cardiac Fibroblast Drives Post-Infarction Cardiac Remodeling through CtBP1-Associated repression of Nr4a1.iScience · 2026Article
- Beyond EMT: Mesenchymal drift as an emerging driver of stromal-immune reprogramming in prostate cancer.iScience · 2026Review
- Whole-genome sequencing implicates rare, low-frequency and structural non-coding variation at themedRxiv : the preprint server for health sciences · 2026Article
- Targeting bromodomain and extraterminal proteins in cardiovascular disease: Pathological mechanisms and therapeutic applications.The Journal of international medical research · 2026Review
- Intercellular chemerin-cmklr1 couples epicardial mechanosensing to fibroblasts in pressure overload.Nature communications · 2026Article
- ACAD8 deficiency promotes pathological cardiac hypertrophy in response to pressure overload by regulating histone isobutyrylation.Nature communications · 2026Article
- γδ T cell-stromal networks modulate matrix composition and vascularity in foreign body response.Nature communications · 2026Article
- VAP1 promotes cardiac fibrosis by enabling PDGFR signaling in myofibroblasts.Experimental & molecular medicine · 2026Article
- Sympathetic-like-integrated engineered heart tissue models AGEs-induced adverse remodeling.Cardiovascular diabetology · 2026Article
- IFNγ-induced antigen loss in chimeric antigen receptor-T cell therapy.Frontiers in immunology · 2026Article
- Integrating Senescence and Oxidative Stress in Cardiac Disease.International journal of molecular sciences · 2025Review
- 3-D biomechanics and epigenomics reveal atypical fibroblast responses in cardiometabolic disease.American journal of physiology. Heart and circulatory physiology · 2025Article
- S-nitrosylation of paired-related homeobox 1 promotes cardiac remodeling following myocardial infarction.Redox biology · 2025Article
- Multi-ancestry Genome-wide Association Study of Inpatient Opioid Dosing Following Knee or Hip Arthroplasty.Research square · 2025Article
- Wnt/β-catenin pathway induces cardiac dysfunction via AKAP6-mediated RyR2 phosphorylation and sarcoplasmic reticulum calcium leakage.Journal of molecular cell biology · 2025Article
- Multi-ancestry Genome-wide Association Study of Inpatient Opioid Dosing Following Knee or Hip Arthroplasty.medRxiv : the preprint server for health sciences · 2025Article
- scCompass: An Integrated Multi-Species scRNA-seq Database for AI-Ready.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- FXYD2 marks and regulates maturity of β cells via ion channel-mediated signal transduction.Nature communications · 2025Article
- IL-22 Attenuates Pressure Overload-Induced Heart Failure and Inflammation.Journal of cardiovascular translational research · 2025Article
Corrections and comments
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Authors and funding
19 authors at 2 institutions in 2 countries.
Funding
Abstract
Cardiac fibroblasts (CFs) are the primary cells tasked with depositing and remodeling collagen and significantly associated with heart failure (HF). TEAD1 has been shown to be essential for heart development and homeostasis. However, fibroblast endogenous TEAD1 in cardiac remodeling remains incompletely understood. Transcriptomic analyses revealed consistently upregulated cardiac TEAD1 expression in mice 4 weeks after transverse aortic constriction (TAC) and Ang-II infusion. Further investigation revealed that CFs were the primary cell type expressing elevated TEAD1 levels in response to pressure overload. Conditional TEAD1 knockout was achieved by crossing TEAD1-floxed mice with CFs- and myofibroblasts-specific Cre mice. Echocardiographic and histological analyses demonstrated that CFs- and myofibroblasts-specific TEAD1 deficiency and treatment with TEAD1 inhibitor, VT103, ameliorated TAC-induced cardiac remodeling. Mechanistically, RNA-seq and ChIP-seq analysis identified Wnt4 as a novel TEAD1 target. TEAD1 has been shown to promote the fibroblast-to-myofibroblast transition through the Wnt signalling pathway, and genetic Wnt4 knockdown inhibited the pro-transformation phenotype in CFs with TEAD1 overexpression. Furthermore, co-immunoprecipitation combined with mass spectrometry, chromatin immunoprecipitation, and luciferase assays demonstrated interaction between TEAD1 and BET protein BRD4, leading to the binding and activation of the Wnt4 promoter. In conclusion, TEAD1 is an essential regulator of the pro-fibrotic CFs phenotype associated with pathological cardiac remodeling via the BRD4/Wnt4 signalling pathway.
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Registered trials
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