ArticleJCI insight2018
Acetylation contributes to hypertrophy-caused maturational delay of cardiac energy metabolism.
Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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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
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- Cardiac energy substrate utilization in heart failure with preserved ejection fraction: reconciling conflicting evidence on fatty acid and glucose metabolism.American journal of physiology. Heart and circulatory physiology · 2025Pooled it
- NADMetabolites · 2025Article
- Pyruvate dehydrogenase kinase 1 controls triacylglycerol hydrolysis in cardiomyocytes.bioRxiv : the preprint server for biology · 2025Article
- Energy metabolism in health and diseases.Signal transduction and targeted therapy · 2025Review
- Article
- Dapagliflozin prevents ERK activation and SGLT2-dependent endoglin upregulation in a mechanically provoked cardiac injury model.Physiological reports · 2024Article
- Comparative Metabolomics in Single Ventricle Patients after Fontan Palliation: A Strong Case for a Targeted Metabolic Therapy.Metabolites · 2023Review
- Failure to Launch: Impaired Cardiac Mitochondrial Metabolic Development in Newborns With Single Ventricle Heart Failure.JACC. Basic to translational science · 2023Article
- Energy Metabolism on Mitochondrial Maturation and Its Effects on Cardiomyocyte Cell Fate.Frontiers in cell and developmental biology · 2022Review
- Emerging Roles of SIRT3 in Cardiac Metabolism.Frontiers in cardiovascular medicine · 2022Review
- Role of Posttranslational Modifications of Proteins in Cardiovascular Disease.Oxidative medicine and cellular longevity · 2022Review
- Post-translational Acetylation Control of Cardiac Energy Metabolism.Frontiers in cardiovascular medicine · 2021Review
- Goals in Nutrition Science 2020-2025.Frontiers in nutrition · 2020Review
- Increased ketone body oxidation provides additional energy for the failing heart without improving cardiac efficiency.Cardiovascular research · 2019Article
- Mitochondria-Targeting Antioxidant Provides Cardioprotection through Regulation of Cytosolic and Mitochondrial ZnInternational journal of molecular sciences · 2019Article
- The protein acetylase GCN5L1 modulates hepatic fatty acid oxidation activity via acetylation of the mitochondrial β-oxidation enzyme HADHA.The Journal of biological chemistry · 2018Article
- Empagliflozin Increases Cardiac Energy Production in Diabetes: Novel Translational Insights Into the Heart Failure Benefits of SGLT2 Inhibitors.JACC. Basic to translational science · 2018 · on this mapArticle
- Mitochondrial dysfunction in pathophysiology of heart failure.The Journal of clinical investigation · 2018Review
Corrections and comments
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Authors and funding
12 authors at 1 institution in 2 countries.
Funding
Abstract
A dramatic increase in cardiac fatty acid oxidation occurs following birth. However, cardiac hypertrophy secondary to congenital heart diseases (CHDs) delays this process, thereby decreasing cardiac energetic capacity and function. Cardiac lysine acetylation is involved in modulating fatty acid oxidation. We thus investigated what effect cardiac hypertrophy has on protein acetylation during maturation. Eighty-four right ventricular biopsies were collected from CHD patients and stratified according to age and the absence (n = 44) or presence of hypertrophy (n = 40). A maturational increase in protein acetylation was evident in nonhypertrophied hearts but not in hypertrophied hearts. The fatty acid β-oxidation enzymes, long-chain acyl CoA dehydrogenase (LCAD) and β-hydroxyacyl CoA dehydrogenase (βHAD), were hyperacetylated and their activities positively correlated with their acetylation after birth in nonhypertrophied hearts but not hypertrophied hearts. In line with this, decreased cardiac fatty acid oxidation and reduced acetylation of LCAD and βHAD occurred in newborn rabbits subjected to cardiac hypertrophy due to an aortocaval shunt. Silencing the mRNA of general control of amino acid synthesis 5-like protein 1 reduced acetylation of LCAD and βHAD as well as fatty acid oxidation rates in cardiomyocytes. Thus, hypertrophy in CHDs prevents the postnatal increase in myocardial acetylation, resulting in a delayed maturation of cardiac fatty acid oxidation.
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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.