ArticleExperimental & molecular medicine2019
Inhibition of acetylation of histones 3 and 4 attenuates aortic valve calcification.
Article in Experimental & molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 21 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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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
21 citing papers in PubMed, 37 citations in OpenAlex.
- Crosstalk between ubiquitination and other post-translational modifications in cardiovascular diseases.iScience · 2026Review
- Reversion of aortic valve cells calcification by activation of Notch signalling via histone acetylation induction.Signal transduction and targeted therapy · 2025Article
- Bibliometric analysis of treatment modalities in calcific aortic valve stenosis.Frontiers in pharmacology · 2025Article
- Role of histone post-translational modifications in atherosclerosis and the therapeutic potential of targeting epigenetic modifiers.Frontiers in cell and developmental biology · 2025Review
- The role and mechanism of protein post‑translational modification in vascular calcification (Review).Experimental and therapeutic medicine · 2024Review
- Review
- DNA methylation and histone post-translational modifications in atherosclerosis and a novel perspective for epigenetic therapy.Cell communication and signaling : CCS · 2023Review
- Vascular calcification: from the perspective of crosstalk.Molecular biomedicine · 2023Review
- Extracellular matrix stiffness controls cardiac valve myofibroblast activation through epigenetic remodeling.Bioengineering & translational medicine · 2022Article
- Senescence mechanisms and targets in the heart.Cardiovascular research · 2022Review
- SPARC-related modular calcium binding 1 regulates aortic valve calcification by disrupting BMPR-II/p-p38 signalling.Cardiovascular research · 2022Article
- Role of endothelial cells in vascular calcification.Frontiers in cardiovascular medicine · 2022Review
- Mammalian Sirtuins and Their Relevance in Vascular Calcification.Frontiers in pharmacology · 2022Review
- Perspectives on pediatric congenital aortic valve stenosis: Extracellular matrix proteins, post translational modifications, and proteomic strategies.Frontiers in cardiovascular medicine · 2022Review
- Towards Personalized Therapy of Aortic Stenosis.Journal of personalized medicine · 2021Review
- Review
- Telocytes-derived extracellular vesicles alleviate aortic valve calcification by carrying miR-30b.ESC heart failure · 2021Article
- The Complex Interplay of Inflammation, Metabolism, Epigenetics, and Sex in Calcific Disease of the Aortic Valve.Frontiers in cardiovascular medicine · 2021Review
- Upregulated microRNA‑330‑3p promotes calcification in the bicuspid aortic valve via targeting CREBBP.Molecular medicine reports · 2020Article
- Roles of Histone Acetylation Modifiers and Other Epigenetic Regulators in Vascular Calcification.International journal of molecular sciences · 2020Review
Corrections and comments
- Erratum issued
- Retracted
Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
Aortic valve calcification develops in patients with chronic kidney disease who have calcium and phosphate metabolic disorders and poor prognoses. There is no effective treatment except valve replacement. However, metabolic disorders put patients at high risk for surgery. Increased acetylation of histones 3 and 4 is present in interstitial cells from human calcific aortic valves, but whether it is involved in aortic valve calcification has not been studied. In this study, we found that treating cultured porcine aortic valve interstitial cells with a high-calcium/high-phosphate medium induced calcium deposition, apoptosis, and expression of osteogenic marker genes, producing a phenotype resembling valve calcification in vivo. These phenotypic changes were attenuated by the histone acetyltransferase inhibitor C646. C646 treatment increased the levels of class I histone deacetylase members and decreased the acetylation of histones 3 and 4 induced by the high-calcium/high-phosphate treatment. Conversely, the histone deacetylase inhibitor suberoylanilide hydroxamic acid promoted valve interstitial cell calcification. In a mouse model of aortic valve calcification induced by adenine and vitamin D treatment, the levels of acetylated histones 3 and 4 were increased in the calcified aortic valves. Treatment of the models with C646 attenuated aortic valve calcification by restoring the levels of acetylated histones 3 and 4. These observations suggest that increased acetylation of histones 3 and 4 is part of the pathogenesis of aortic valve calcification associated with calcium and phosphate metabolic disorders. Targeting acetylated histones 3 and 4 may be a potential therapy for inoperable aortic valve calcification in chronic kidney disease patients.
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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.