ArticleJournal of the American Heart Association2020
Histone Acetyltransferase p300 Inhibitor Improves Coronary Flow Reserve in SIRT3 (Sirtuin 3) Knockout Mice.
Article in Journal of the American Heart Association, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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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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Who cites it
28 citing papers in PubMed, 44 citations in OpenAlex.
- Histone Modifications in Cardiovascular Disease: Mechanisms and Therapeutic Opportunities.MedComm · 2026Review
- Mitigation of Injury from Myocardial Infarction by Pentamidine, an Inhibitor of the Acetyltransferase Tip60.Cardiovascular drugs and therapy · 2026Article
- Kuanxiong aerosol protects against coronary microvascular dysfunction through improving angiogenesis via HIF-1α-ITGAX axis.Frontiers in pharmacology · 2026Article
- Epigenetic reprogramming drives endothelial dysfunction via neuropilin-1 in pulmonary hypertension.Molecular medicine (Cambridge, Mass.) · 2025Article
- Sirtuins as Endogenous Regulators of Cardiac Fibrosis: A Current Perspective.Cardiovascular toxicology · 2025Review
- Norepinephrine exacerbates LPS-induced cardiomyopathy via SIRT3/HO-1 axis-mediated ferroptosis.Critical care (London, England) · 2025Article
- Epigenetic Mechanisms in Heart Diseases.Reviews in cardiovascular medicine · 2025Review
- Knockout of Sirtuin 3 in endothelial cells impairs endothelial-dependent relaxation and myogenic response in mice.Physiological reports · 2024Article
- Capsaicin mitigates ventilator-induced lung injury by suppressing ferroptosis and maintaining mitochondrial redox homeostasis through SIRT3-dependent mechanisms.Molecular medicine (Cambridge, Mass.) · 2024Article
- Mouse Cardiovascular Imaging.Current protocols · 2024Review
- Epigenetic regulation of sex dimorphism in cardiovascular health.Canadian journal of physiology and pharmacology · 2024Review
- Endothelial Cell-Specific Prolyl Hydroxylase-2 Deficiency Augments Angiotensin II-Induced Arterial Stiffness and Cardiac Pericyte Recruitment in Mice.Journal of the American Heart Association · 2024Article
- p53 Acetylation Exerts Critical Roles in Pressure Overload-Induced Coronary Microvascular Dysfunction and Heart Failure in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- Molecular mechanisms of endothelial dysfunction in coronary microcirculation dysfunction.Journal of thrombosis and thrombolysis · 2023Review
- Epigenetic Regulation of Fibroblasts and Crosstalk between Cardiomyocytes and Non-Myocyte Cells in Cardiac Fibrosis.Biomolecules · 2023Review
- EP300 as a Molecular Integrator of Fibrotic Transcriptional Programs.International journal of molecular sciences · 2023Review
- SIRT3 Deficiency Enhances Ferroptosis and Promotes Cardiac Fibrosis via p53 Acetylation.Cells · 2023Article
- Pharmacological inhibition of the acetyltransferase Tip60 mitigates myocardial infarction injury.Disease models & mechanisms · 2023Article
- Emerging epigenetic therapies of cardiac fibrosis and remodelling in heart failure: from basic mechanisms to early clinical development.Cardiovascular research · 2023Review
- Therapeutic targets for cardiac fibrosis: from old school to next-gen.The Journal of clinical investigation · 2022Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Background Coronary microvascular dysfunction is common in patients of myocardial infarction with non-obstructive coronary artery disease. Coronary flow reserve (CFR) reflects coronary microvascular function and is a powerful independent index of coronary microvascular dysfunction and heart failure. Our previous studies showed that knockout of SIRT3 (Sirtuin 3) decreased CFR and caused a diastolic dysfunction. Few studies focus on the treatment of impaired CFR and heart failure. In the present study, we explored the role of C646, a histone acetyltransferase p300 inhibitor, in regulating CFR and cardiac remodeling in SIRT3 knockout (SIRT3KO) mice. Methods and Results After treating with C646 for 14 days, CFR, pulse-wave velocity, and cardiac function were measured in SIRT3KO mice. SIRT3KO mice treated with C646 showed a significant improvement of CFR, pulse-wave velocity, ejection fraction, and fractional shortening. Treatment with C646 reversed pre-existing cardiac fibrosis, hypertrophy, and capillary rarefaction in SIRT3KO mice. Mechanistically, knockout of Sirtuin 3 resulted in significant increases in p300 expression and H3K56 acetylation. Treatment with C646 significantly reduced levels of p300 and H3K56 acetylation in SIRT3KO mice. Furthermore, treatment with C646 increased endothelial nitric oxide synthase expression and reduced arginase II expression and activity. The expression of NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) and VCAM-1 (vascular cell adhesion molecule 1) was also significantly suppressed by C646 treatment in SIRT3KO mice. Conclusions C646 treatment attenuated p300 and H3K56 acetylation and improved arterial stiffness and CFR via improvement of endothelial cell (EC) dysfunction and suppression of NF-κB.
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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.