ArticlePhysiological reports2022
GCN5L1 impairs diastolic function in mice exposed to a high fat diet by restricting cardiac pyruvate oxidation.
Article in Physiological reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- BLOC1S1 variants cause lysosomal and autophagic defects resulting in a hypomyelinating leukodystrophy with epileptic encephalopathy.American journal of human genetics · 2026Article
- Article
- Sex-dependent effects of a high-fat diet-induced obesity model on cerebrovascular health and brain metabolism.Experimental physiology · 2025Article
- GCN5L1 Inhibits Pyruvate Dehydrogenase Phosphorylation During Cardiac Ischemia-Reperfusion Injury.FASEB bioAdvances · 2025Article
- Mitochondrial Dysfunction in HFpEF: Potential Interventions Through Exercise.Journal of cardiovascular translational research · 2025Review
- Deciphering the Role of Copper Homeostasis in Atherosclerosis: From Molecular Mechanisms to Therapeutic Targets.International journal of molecular sciences · 2024Review
- Post-translational modifications of pyruvate dehydrogenase complex in cardiovascular disease.iScience · 2024Review
- Validation of GCN5L1/BLOC1S1/BLOS1 antibodies using knockout cells and tissue.The Biochemical journal · 2024Article
- Protein lysine acetylation does not contribute to the high rates of fatty acid oxidation seen in the post-ischemic heart.Scientific reports · 2024Article
- Animal models of heart failure with preserved ejection fraction (HFpEF): from metabolic pathobiology to drug discovery.Acta pharmacologica Sinica · 2024Review
- The role of acetylation in obesity-induced cardiac metabolic alterations.Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques · 2024Review
- Fibroblast-to-cardiomyocyte lactate shuttle modulates hypertensive cardiac remodelling.Cell & bioscience · 2023Article
- GCN5L1 impairs diastolic function in mice exposed to a high fat diet by restricting cardiac pyruvate oxidation.Physiological reports · 2022Article
- Maternal obesity and the impact of associated early-life inflammation on long-term health of offspring.Frontiers in cellular and infection microbiology · 2022Review
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
Left ventricular diastolic dysfunction is a structural and functional condition that precedes the development of heart failure with preserved ejection fraction (HFpEF). The etiology of diastolic dysfunction includes alterations in fuel substrate metabolism that negatively impact cardiac bioenergetics, and may precipitate the eventual transition to heart failure. To date, the molecular mechanisms that regulate early changes in fuel metabolism leading to diastolic dysfunction remain unclear. In this report, we use a diet-induced obesity model in aged mice to show that inhibitory lysine acetylation of the pyruvate dehydrogenase (PDH) complex promotes energetic deficits that may contribute to the development of diastolic dysfunction in mouse hearts. Cardiomyocyte-specific deletion of the mitochondrial lysine acetylation regulatory protein GCN5L1 prevented hyperacetylation of the PDH complex subunit PDHA1, allowing aged obese mice to continue using pyruvate as a bioenergetic substrate in the heart. Our findings suggest that changes in mitochondrial protein lysine acetylation represent a key metabolic component of diastolic dysfunction that precedes 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.