ArticleThe Journal of clinical investigation2022
YAP mediates compensatory cardiac hypertrophy through aerobic glycolysis in response to pressure overload.
Article in The Journal of clinical investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
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Who cites it
79 citing papers in PubMed, 155 citations in OpenAlex.
- Bidirectional metabolic-vascular feedback loops in heart failure: From myocardial energetics to multisystem cardiometabolic crosstalk.iScience · 2026Review
- YAP and WWTR1/TAZ Connect Mechanotransduction and Mitochondrial Metabolism in Cardiac Hypertrophy and Ventricular Remodeling.Journal of cardiovascular translational research · 2026Review
- AMOT mediates YAP1 activation and promotes the cell progression and glycolysis in non-small cell lung cancer by modulating the Hippo signaling pathway.Translational cancer research · 2026Article
- Cardiac fibrosis: mechanistic insights and translational advances.Molecular biomedicine · 2026Review
- Failure of morphogenesis in chronic inflammation-associated early tumourigenesis: Extracellular matrix biomechanics as an integrative layer.Biochemistry and biophysics reports · 2026Review
- The E3 Ligase RNF115 Aggravates Pathological Cardiac Hypertrophy via Ubiquitin-Mediated Degradation of SPTBN1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Creatine metabolism regulates trophectoderm formation in early mouse embryos via an energy-cytoskeleton-YAP axis.The Journal of biological chemistry · 2026Article
- Targeting YAP: mechanistic breakthroughs and therapeutic prospects in reversing organ fibrosis.Molecular and cellular biochemistry · 2026Review
- Article
- Reduced Myocardial Serine Synthesis Impairs Functional, Metabolic, and Redox Adaptations to Cardiac Stress.bioRxiv : the preprint server for biology · 2026Article
- Cardiac mechanotransduction from development to disease.APL bioengineering · 2026Review
- Metabolic inflexibility across heart failure phenotypes: mechanisms and type-specific therapeutic implications.Apoptosis : an international journal on programmed cell death · 2026Review
- Metabolic maintenance of breast cancer cells and metastases through E-cadherin/YAP-dependent pyruvate carboxylase expression.bioRxiv : the preprint server for biology · 2026Article
- YAP Induces a Prorenewal Metabolic State in Cardiomyocytes.Circulation · 2026Article
- PANK4 Regulates YAP to Modulate the Glycolytic Pathway in LEC for Driving LECs-EMT in Early Diabetic Cataract Pathogenesis.Investigative ophthalmology & visual science · 2026Article
- The Metabolic Role of Mitochondria in the Perinatal Cardiac Development and Cardiovascular Diseases.Exploration (Beijing, China) · 2026Review
- YAP1 in control: how RNA networks and protein modifications shape its function and therapeutic targetability.Molecular cancer · 2026Review
- Solute Carrier transporters in tumor metabolism and immune modulation: implications for therapy.Journal of translational medicine · 2026Review
- Beyond Catalytic Therapy: Copper-Paeonol Nanozymes Disrupt Fascin-Mediated Actin Bundling to Suppress Tumor Growth and Metastasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Microglial Fkbp5 Impairs Post-Stroke Vascular Integrity and Regeneration by Promoting Yap1-Mediated Glycolysis and Oxidative Phosphorylation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
19 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
The heart utilizes multiple adaptive mechanisms to maintain pump function. Compensatory cardiac hypertrophy reduces wall stress and oxygen consumption, thereby protecting the heart against acute blood pressure elevation. The nuclear effector of the Hippo pathway, Yes-associated protein 1 (YAP), is activated and mediates compensatory cardiac hypertrophy in response to acute pressure overload (PO). In this study, YAP promoted glycolysis by upregulating glucose transporter 1 (GLUT1), which in turn caused accumulation of intermediates and metabolites of the glycolytic, auxiliary, and anaplerotic pathways during acute PO. Cardiac hypertrophy was inhibited and heart failure was exacerbated in mice with YAP haploinsufficiency in the presence of acute PO. However, normalization of GLUT1 rescued the detrimental phenotype. PO induced the accumulation of glycolytic metabolites, including l-serine, l-aspartate, and malate, in a YAP-dependent manner, thereby promoting cardiac hypertrophy. YAP upregulated the GLUT1 gene through interaction with TEA domain family member 1 (TEAD1) and HIF-1α in cardiomyocytes. Thus, YAP induces compensatory cardiac hypertrophy through activation of the Warburg effect.
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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.