ArticleeLife2021
Acetyl-CoA production by specific metabolites promotes cardiac repair after myocardial infarction via histone acetylation.
Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 51 citations in OpenAlex.
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- Mitochondrial targets in ischaemic heart disease and heart failure, and their potential for a more efficient clinical translation. A scientific statement of the ESC Working Group on Cellular Biology of the Heart and the ESC Working Group on Myocardial Function.European journal of heart failure · 2025Review
- Molecular interplay of ARID1A in gastrointestinal cancers.Medical oncology (Northwood, London, England) · 2025Review
- Epi-nutrients for cancer prevention: Molecular mechanisms and emerging insights.Cell biology and toxicology · 2025Review
- The Fundamental Role of Nutrients for Metabolic Balance and Epigenome Integrity Maintenance.Epigenomes · 2025Review
- cIAP2-mediated IGF2BP2 ubiquitination and degradation regulate cardiomyocyte apoptosis via stabilizing mCell biology and toxicology · 2025Article
- Exosome-based immunotherapy in hepatocellular carcinoma.Clinical and experimental medicine · 2025Review
- Association between different obesity metrics and risk of inguinal hernia.Updates in surgery · 2025Article
- Programmed cardiomyocyte death in myocardial infarction.Apoptosis : an international journal on programmed cell death · 2025Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Myocardial infarction (MI) is accompanied by severe energy deprivation and extensive epigenetic changes. However, how energy metabolism and chromatin modifications are interlinked during MI and heart repair has been poorly explored. Here, we examined the effect of different carbon sources that are involved in the major metabolic pathways of acetyl-CoA synthesis on myocardial infarction and found that elevation of acetyl-CoA by sodium octanoate (8C) significantly improved heart function in ischemia reperfusion (I/R) rats. Mechanistically, 8C reduced I/R injury by promoting histone acetylation which in turn activated the expression of antioxidant genes and inhibited cardiomyocyte (CM) apoptosis. Furthermore, we elucidated that 8C-promoted histone acetylation and heart repair were carried out by metabolic enzyme medium-chain acyl-CoA dehydrogenase (MCAD) and histone acetyltransferase Kat2a, suggesting that 8C dramatically improves cardiac function mainly through metabolic acetyl-CoA-mediated histone acetylation. Therefore, our study uncovers an interlinked metabolic/epigenetic network comprising 8C, acetyl-CoA, MCAD, and Kat2a to combat heart injury.
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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.