ArticleAmerican journal of physiology. Heart and circulatory physiology2025
Cardiomyocyte YAP represses myocardial inflammation and fibrosis and restrains MEF2-regulated gene expression.
Article in American journal of physiology. Heart and circulatory physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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
6 citing papers in PubMed.
- Hippo Pathway-YAP/TAZ Signaling: Molecular Mechanisms, Biological Function, Diseases, and Therapeutic Targets.MedComm · 2026Review
- YAP Induces a Prorenewal Metabolic State in Cardiomyocytes.Circulation · 2026Article
- Potential Cardioprotective Effect of a GRK5 Inhibitor Against NF-κB-Mediated Inflammation in an Animal Model of Isoproterenol-Induced Myocardial Infarction.International journal of molecular sciences · 2025Article
- Integrating Senescence and Oxidative Stress in Cardiac Disease.International journal of molecular sciences · 2025Review
- Cardiomyocytes regulate Inflammation in the failing heart.American journal of physiology. Heart and circulatory physiology · 2025Article
- Cardiomyocyte YAP represses myocardial inflammation and fibrosis and restrains MEF2-regulated gene expression.American journal of physiology. Heart and circulatory physiology · 2025Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Cardiomyocyte signaling through the transcriptional coactivator Yes-associated protein (YAP) has been shown to protect the myocardium against ischemic or mechanical stress. Inflammatory responses initiated in cardiomyocytes play a major role in the development of cardiac dysfunction. We tested the relationship between YAP and inflammatory gene expression using cardiomyocyte-specific YAP-knockout (KO) mice. Wild-type (WT) and KO mice were infused with angiotensin II (AngII) at 1.5 μg/kg/min and euthanized 24 h or 3 days postinfusion. YAP deletion markedly enhanced AngII-induced mRNA expression of proinflammatory cytokines and chemokines, a response that occurred selectively within cardiomyocytes. Hearts from YAP-KO mice also had increased F4/80, CD68, and Col1 staining. Single-nuclei RNA sequencing of WT and YAP-KO hearts showed significant upregulation of proinflammatory cytokines and of a range of genes, including those in the
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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 Socratic graph.