ArticleCirculation2008
Quantitative control of adaptive cardiac hypertrophy by acetyltransferase p300.
Article in Circulation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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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
68 citing papers in PubMed, 132 citations in OpenAlex.
- Research progress on lysine acetylation (Review).International journal of molecular medicine · 2026Review
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- Epigenetic Regulation and Molecular Mechanisms in Cardiovascular Diseases: A Review of Recent Advances and Therapeutic Implications.International journal of molecular sciences · 2026Review
- Peroxisome Proliferator-Activated Receptor Family of Lipid-Activated Nuclear Receptors Alpha Silencing Promotes Oxidative Stress and Hypertrophic Phenotype in Rat Cardiac Cells.Antioxidants (Basel, Switzerland) · 2025Article
- Review
- Unraveling the metabolic‒epigenetic nexus: a new frontier in cardiovascular disease treatment.Cell death & disease · 2025Review
- Caloric restriction and its mimetics in heart failure with preserved ejection fraction: mechanisms and therapeutic potential.Cardiovascular diabetology · 2025Review
- Downregulation of MLF1 safeguards cardiomyocytes against senescence-associated chromatin opening.Nucleic acids research · 2025Article
- Microtubules Sequester Acetylated YAP in the Cytoplasm and Inhibit Heart Regeneration.Circulation · 2025Article
- Review
- Anserine, a Histidine-Containing Dipeptide, Suppresses Pressure Overload-Induced Systolic Dysfunction by Inhibiting Histone Acetyltransferase Activity of p300 in Mice.International journal of molecular sciences · 2024Article
- Article
- Identification and Characterization of p300-Mediated Lysine Residues in Cardiac SERCA2a.International journal of molecular sciences · 2023Article
- Emerging epigenetic therapies of cardiac fibrosis and remodelling in heart failure: from basic mechanisms to early clinical development.Cardiovascular research · 2023Review
- Roles of histone acetylation sites in cardiac hypertrophy and heart failure.Frontiers in cardiovascular medicine · 2023Review
- Acetyltransferase p300 regulates atrial fibroblast senescence and age-related atrial fibrosis through p53/Smad3 axis.Aging cell · 2023Article
- Mechanism of histone deacetylases in cardiac hypertrophy and its therapeutic inhibitors.Frontiers in cardiovascular medicine · 2022Review
- Multimerization of the GATA4 transcription factor regulates transcriptional activity and cardiomyocyte hypertrophic response.International journal of biological sciences · 2022Article
- MIAT, a potent CVD-promoting lncRNA.Cellular and molecular life sciences : CMLS · 2021Article
- Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAcetyltransferase p300 is essential for cardiac development and is thought to be involved in cardiac myocyte growth through MEF2- and GATA4-dependent transcription. However, the importance of p300 in the modulation of cardiac growth in vivo is unknown. METHODS AND
resultsPressure overload induced by transverse aortic coarctation, postnatal physiological growth, and human heart failure were associated with large increases in p300. Minimal transgenic overexpression of p300 (1.5- to 3.5-fold) induced striking myocyte and cardiac hypertrophy. Both mortality and cardiac mass were directly related to p300 protein dosage. Heterozygous loss of a single p300 allele reduced pressure overload-induced hypertrophy by approximately 50% and rescued the hypertrophic phenotype of p300 overexpressers. Increased p300 expression had no effect on total histone deacetylase activity but was associated with proportional increases in p300 acetyltransferase activity and acetylation of the p300 substrates histone 3 and GATA-4. Remarkably, a doubling of p300 levels was associated with the de novo acetylation of MEF2. Consistent with this, genes specifically upregulated in p300 transgenic hearts were highly enriched for MEF2 binding sites.
conclusionsSmall increments in p300 are necessary and sufficient to drive myocardial hypertrophy, possibly through acetylation of MEF2 and upstream of signals promoting phosphorylation or nuclear export of histone deacetylases. We propose that induction of myocardial p300 content is a primary rate-limiting event in the response to hemodynamic loading in vivo and that p300 availability drives and constrains adaptive myocardial growth. Specific reduction of p300 content or activity may diminish stress-induced hypertrophy and forestall the development of 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.