ArticleThe Journal of biological chemistry2019
Yes-associated protein (YAP) mediates adaptive cardiac hypertrophy in response to pressure overload.
Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 91 citations in OpenAlex.
- YAP and WWTR1/TAZ Connect Mechanotransduction and Mitochondrial Metabolism in Cardiac Hypertrophy and Ventricular Remodeling.Journal of cardiovascular translational research · 2026Review
- Cardiac fibrosis: mechanistic insights and translational advances.Molecular biomedicine · 2026Review
- The E3 Ligase RNF115 Aggravates Pathological Cardiac Hypertrophy via Ubiquitin-Mediated Degradation of SPTBN1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- MAP4K4 inhibition enhances the anti-ferroptosis effect of the FTO/YAP/ATF4 axis in doxorubicin-induced cardiotoxicity.Cell biology and toxicology · 2026Article
- Mechanobiology-Driven Metabolic Reprogramming: Integrative Roles of YAP/TAZ Signaling and Extracellular Matrix Dynamics.Cell biology international · 2026Review
- Cardiac mechanotransduction from development to disease.APL bioengineering · 2026Review
- Dimethyl Fumarate Reverses β-Adrenoceptor-Mediated Myocardial Fibrosis in Mice by Inhibiting Yes-Associated Protein-Regulated Expression of Intermediate-Conductance CaJournal of the American Heart Association · 2026Article
- YAP1 reactivation in cardiomyocytes following ECM remodelling contributes to the development of contractile force and sarcomere maturation.Cell death discovery · 2025Article
- Cardiac hypertrophy at the crossroads: Mechanistic insights and emerging multimodal therapeutic strategies.European journal of pharmacology · 2025Review
- Molecular gatekeepers of endogenous adult mammalian cardiomyocyte proliferation.Nature reviews. Cardiology · 2025Review
- Cell type specificity of Hippo-YAP signaling in cardiac development and disease.Journal of molecular and cellular cardiology · 2025Review
- Cardiomyocyte YAP represses myocardial inflammation and fibrosis and restrains MEF2-regulated gene expression.American journal of physiology. Heart and circulatory physiology · 2025Article
- Crosstalk between MST1-Hippo and Wnt/β-Catenin, Notch, and PI3K/Akt pathways in cardiac physiology and pathology.Journal of physiology and biochemistry · 2025Review
- Hippo Pathway Regulates Cell Proliferation in Skin Epidermis Exposed to Mechanical Forces.Journal of cellular and molecular medicine · 2025Article
- The Mechanical Role of YAP/TAZ in the Development of Diabetic Cardiomyopathy.Current issues in molecular biology · 2025Review
- The role of mechanosignaling in the control of myocardial mass.American journal of physiology. Heart and circulatory physiology · 2025Review
- Verteporfin Mitigates Isoproterenol-Induced Myocardial Hypertrophy by Attenuating IL-6/STAT3 in Cardiac Fibroblasts.Cardiovascular therapeutics · 2025Article
- The Multifaceted Roles of Hippo-YAP in Cardiovascular Diseases.Cardiovascular toxicology · 2024Review
- YAP/TAZ as mechanobiological signaling pathway in cardiovascular physiological regulation and pathogenesis.Mechanobiology in medicine · 2024Article
- Research trends and hotspots of circular RNA in cardiovascular disease: A bibliometric analysis.Non-coding RNA research · 2024Article
10 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Cardiovascular disease (CVD) remains the leading cause of death globally, and heart failure is a major component of CVD-related morbidity and mortality. The development of cardiac hypertrophy in response to hemodynamic overload is initially considered to be beneficial; however, this adaptive response is limited and, in the presence of prolonged stress, will transition to heart failure. Yes-associated protein (YAP), the central downstream effector of the Hippo signaling pathway, regulates proliferation and survival in mammalian cells. Our previous work demonstrated that cardiac-specific loss of YAP leads to increased cardiomyocyte (CM) apoptosis and impaired CM hypertrophy during chronic myocardial infarction (MI) in the mouse heart. Because of its documented cardioprotective effects, we sought to determine the importance of YAP in response to acute pressure overload (PO). Our results indicate that endogenous YAP is activated in the heart during acute PO. YAP activation that depended upon RhoA was also observed in CMs subjected to cyclic stretch. To examine the function of endogenous YAP during acute PO,
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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.