ArticleThe Journal of clinical investigation2023
Reducing branched-chain amino acids improves cardiac stress response in mice by decreasing histone H3K23 propionylation.
Article in The Journal of clinical investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- Propionic acidemia as a framework for understanding the impact of disturbed propionyl-CoA on histone modifications.Biochemical Society transactions · 2026Review
- Precision metabolic therapy for propionic acidemia.Biochemical pharmacology · 2026Review
- ACAD8 deficiency promotes pathological cardiac hypertrophy in response to pressure overload by regulating histone isobutyrylation.Nature communications · 2026Article
- Acetyl-CoA Synthetase 1 regulates global histone propionylation and metabolic stress responses.bioRxiv : the preprint server for biology · 2026Article
- Dietary intake and BCAA metabolism regulate pulmonary fibrosis through KDM4A-mediated epigenetic remodeling in male mice.Nature communications · 2026Article
- Lysine Propionylation as a Metabolically Coupled PTM: Mechanisms, Functional Consequences, and Therapeutic Potentials.International journal of molecular sciences · 2026Review
- H4K16 acylations destabilize chromatin architecture and facilitate transcriptional response during metabolic perturbations.Molecular cell · 2026Article
- Role of Gut Microbiota in Diabetic HFpEF: Mechanisms and Therapeutic Implications.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
- Vascular Smooth Muscle Cell-Specific BCAT2 Deficiency Attenuates Diabetic Atherosclerotic Calcification via Histone Propionylation.Research (Washington, D.C.) · 2026Article
- Post-translational acylation of proteins in cardiac hypertrophy.Nature reviews. Cardiology · 2025Review
- Cardiac intermediary metabolism in heart failure: substrate use, signalling roles and therapeutic targets.Nature reviews. Cardiology · 2025Review
- The regulatory role of exercise in heart failure and myocardial energy metabolism: A review.Biomolecules & biomedicine · 2025Review
- Atlas of lysine propionylation of human right atrium and ALDH6A1-NADH pathway in new-onset atrial fibrillation after coronary surgery.Communications biology · 2025Article
- Cardiometabolic disease management: influences from epigenetics.Epigenomics · 2025Review
- Post-translational modifications of collagen and its related diseases in metabolic pathways.Acta pharmaceutica Sinica. B · 2025Review
- Dietary Branched-Chain Amino Acids Modify Postinfarct Cardiac Remodeling and Function in the Murine Heart.Journal of the American Heart Association · 2025Article
- Metabolism-driven chromatin dynamics: Molecular principles and technological advances.Molecular cell · 2025Review
- Mechanisms of gut microbiota in host fat deposition: metabolites, signaling pathways, and translational applications.Frontiers in microbiology · 2025Review
- The gut microbiota-inflammation-HFpEF axis: deciphering the role of gut microbiota dysregulation in the pathogenesis and management of HFpEF.Frontiers in cellular and infection microbiology · 2025Review
- Divergent roles for propionate and butyrate in colorectal cancer epigenetics.Nature metabolism · 2025Article
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Abstract
Identification of branched-chain amino acid (BCAA) oxidation enzymes in the nucleus led us to predict that they are a source of the propionyl-CoA that is utilized for histone propionylation and, thereby, regulate gene expression. To investigate the effects of BCAAs on the development of cardiac hypertrophy and failure, we applied pressure overload on the heart in mice maintained on a diet with standard levels of BCAAs (BCAA control) versus a BCAA-free diet. The former was associated with an increase in histone H3K23-propionyl (H3K23Pr) at the promoters of upregulated genes (e.g., cell signaling and extracellular matrix genes) and a decrease at the promoters of downregulated genes (e.g., electron transfer complex [ETC I-V] and metabolic genes). Intriguingly, the BCAA-free diet tempered the increases in promoter H3K23Pr, thus reducing collagen gene expression and fibrosis during cardiac hypertrophy. Conversely, the BCAA-free diet inhibited the reductions in promoter H3K23Pr and abolished the downregulation of ETC I-V subunits, enhanced mitochondrial respiration, and curbed the progression of cardiac hypertrophy. Thus, lowering the intake of BCAAs reduced pressure overload-induced changes in histone propionylation-dependent gene expression in the heart, which retarded the development of cardiomyopathy.
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