ArticleBasic research in cardiology2020
TRPV4 deletion protects heart from myocardial infarction-induced adverse remodeling via modulation of cardiac fibroblast differentiation.
Article in Basic research in cardiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 90 citations in OpenAlex.
- Mitochondrial heterogeneity across cardiac cell types in heart failure with preserved ejection fraction.Redox biology · 2026Review
- Multiple triggering mechanisms of myocardial fibrosis: Comparison and integration in different disease contexts.iScience · 2026Review
- Nicotine promotes cardiac fibrosis by regulating miR-125b-5p maturation via HNRNPA2B1-mediated METTL14-dependent m⁶A methylation: therapeutic reversal by cinacalcet HCl.Journal of translational medicine · 2026Article
- Hydrogels loaded with different substances for treating heart failure: a promising therapy.Frontiers in cardiovascular medicine · 2026Review
- Ion channels and cardiac disease: mechanisms and functions of a disintegrin and metalloproteases and their substrates.Frontiers in cell and developmental biology · 2026Review
- TRPV4-Mediated Mechanosensing Regulates the Endothelial-to-Mesenchymal Transition: Implications for Atherosclerosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Integration of cAMP and TRPV4 Signaling to Optimize Collagen Remodeling for Management of Fibrosis.Cells · 2025Review
- Primary Cilia Orchestrate Cardiac Pathogenesis: A Central Nexus of Remodeling, Signaling, and Repair.Cell proliferation · 2025Article
- Transient receptor potential vanilloid type 4 channels mediate bladder cancer cell proliferation, migration, and chemoresistance.The Journal of pharmacology and experimental therapeutics · 2025Article
- An Integrated Analysis of Transcriptomics and Metabolomics Elucidates the Role and Mechanism of TRPV4 in Blunt Cardiac Injury.Metabolites · 2025Article
- Mechanosensitive ion channels and inflammation: key links in cellular signal transduction.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Ubiquitin Specific Protease 9X Regulates the Activation of ARK5 and Promotes Progression of Fibrotic Remodeling.JACC. Basic to translational science · 2025Article
- CaBiomedicines · 2025Review
- FGF2 Attenuated Inflammation-Mediated Cardiac Damage: A Novel Mechanistic Insight into the AMPK-FUNDC1-Mitophagy.Research (Washington, D.C.) · 2025Article
- Development, in vitro, and in vivo assessments of PCL-gelatin-βTCP fibrous scaffolds for cardiac regeneration.BioImpacts : BI · 2025Article
- Cardiac Fibroblasts Enhance MMP2 Activity to Suppress Gap Junction Function in Cardiomyocytes.Applied biochemistry and biotechnology · 2024Article
- Mechanosensitive TRPV4 channel guides maturation and organization of the bilayered mammary epithelium.Scientific reports · 2024Article
- Role of mechanically-sensitive cation channels Piezo1 and TRPV4 in trabecular meshwork cell mechanotransduction.Human cell · 2024Review
- TRPV4 Channels Promote Pathological, but Not Physiological, Cardiac Remodeling through the Activation of Calcineurin/NFAT and TRPC6.International journal of molecular sciences · 2024Article
- The Multifaceted Functions of TRPV4 and Calcium Oscillations in Tissue Repair.International journal of molecular sciences · 2024Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Cardiac fibrosis caused by adverse cardiac remodeling following myocardial infarction can eventually lead to heart failure. Although the role of soluble factors such as TGF-β is well studied in cardiac fibrosis following myocardial injury, the physiological role of mechanotransduction is not fully understood. Here, we investigated the molecular mechanism and functional role of TRPV4 mechanotransduction in cardiac fibrosis. TRPV4KO mice, 8 weeks following myocardial infarction (MI), exhibited preserved cardiac function compared to WT mice. Histological analysis demonstrated reduced cardiac fibrosis in TRPV4KO mice. We found that WT CF exhibited hypotonicity-induced calcium influx and extracellular matrix (ECM)-stiffness-dependent differentiation in response to TGF-β1. In contrast, TRPV4KO CF did not display hypotonicity-induced calcium influx and failed to differentiate on high-stiffness ECM gels even in the presence of saturating amounts of TGF-β1. Mechanistically, TRPV4 mediated cardiac fibrotic gene promoter activity and fibroblast differentiation through the activation of the Rho/Rho kinase pathway and the mechanosensitive transcription factor MRTF-A. Our findings suggest that genetic deletion of TRPV4 channels protects heart from adverse cardiac remodeling following MI by modulating Rho/MRTF-A pathway-mediated cardiac fibroblast differentiation and cardiac 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.