ArticleThe Journal of biological chemistry2010
TEAD-1 overexpression in the mouse heart promotes an age-dependent heart dysfunction.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 59 citations in OpenAlex.
- Article
- ACAD8 deficiency promotes pathological cardiac hypertrophy in response to pressure overload by regulating histone isobutyrylation.Nature communications · 2026Article
- YAP1 reactivation in cardiomyocytes following ECM remodelling contributes to the development of contractile force and sarcomere maturation.Cell death discovery · 2025Article
- Cardiac myosin-binding protein-C acts as a tunable load sensor to regulate afterload dependence of ventricular function.American journal of physiology. Heart and circulatory physiology · 2025Article
- 3-D biomechanics and epigenomics reveal atypical fibroblast responses in cardiometabolic disease.American journal of physiology. Heart and circulatory physiology · 2025Article
- Single-cell RNA sequencing reveals the potential role of Postn(+) fibroblasts in promoting the progression of myocardial fibrosis after myocardial infarction.Scientific reports · 2025Article
- Targeting TEAD in cancer.Frontiers in oncology · 2025Review
- Article
- TEA domain transcription factor 1(TEAD1) induces cardiac fibroblasts cells remodeling through BRD4/Wnt4 pathway.Signal transduction and targeted therapy · 2024Article
- Duality of Nrf2 in iron-overload cardiomyopathy.Haematologica · 2023Article
- TEAD1 trapping by the Q353R-Lamin A/C causes dilated cardiomyopathy.Science advances · 2023Article
- Article
- TEAD1 regulates cell proliferation through a pocket-independent transcription repression mechanism.Nucleic acids research · 2022Article
- Multiomic analyses reveal enriched glycolytic processes in β-myosin heavy chain-expressed cardiomyocytes in early cardiac hypertrophy.Journal of molecular and cellular cardiology plus · 2022Article
- Targeting the Hippo pathway in heart repair.Cardiovascular research · 2022Review
- Potential Role of Exercise in Regulating YAP and TAZ During Cardiomyocytes Aging.Current cardiology reviews · 2022Review
- Many chronological aging clocks can be found throughout the epigenome: Implications for quantifying biological aging.Aging cell · 2021Article
- Discovery of a subtype-selective, covalent inhibitor against palmitoylation pocket of TEAD3.Acta pharmaceutica Sinica. B · 2021Article
- TEAD1 protects against necroptosis in postmitotic cardiomyocytes through regulation of nuclear DNA-encoded mitochondrial genes.Cell death and differentiation · 2021Article
- Vezf1 regulates cardiac structure and contractile function.EBioMedicine · 2020Article
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
TEA domain transcription factor-1 (TEAD-1) is essential for proper heart development and is implicated in cardiac specific gene expression and the hypertrophic response of primary cardiomyocytes to hormonal and mechanical stimuli, and its activity increases in the pressure-overloaded hypertrophied rat heart. To investigate whether TEAD-1 is an in vivo modulator of cardiac specific gene expression and hypertrophy, we developed transgenic mice expressing hemagglutinin-tagged TEAD-1 under the control of the muscle creatine kinase promoter. We show that a sustained increase in TEAD-1 protein leads to an age-dependent dysfunction. Magnetic resonance imaging revealed decreases in cardiac output, stroke volume, ejection fraction, and fractional shortening. Isolated TEAD-1 hearts revealed decreased left ventricular power output that correlated with increased betaMyHC protein. Histological analysis showed altered alignment of cardiomyocytes, septal wall thickening, and fibrosis, although electrocardiography displayed a left axis shift of mean electrical axis. Transcripts representing most members of the fetal heart gene program remained elevated from fetal to adult life. Western blot analyses revealed decreases in p-phospholamban, SERCA2a, p-CX43, p-GSK-3alpha/beta, nuclear beta-catenin, GATA4, NFATc3/c4, and increased NCX1, nuclear DYKR1A, and Pur alpha/beta protein. TEAD-1 mice did not display cardiac hypertrophy. TEAD-1 mice do not tolerate stress as they die over a 4-day period after surgical induction of pressure overload. These data provide the first in vivo evidence that increased TEAD-1 can induce characteristics of cardiac remodeling associated with cardiomyopathy and heart failure.
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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.