ArticleMedComm2025
Histone H3 Lysine 18 Lactylation Promotes Cardiac Hypertrophy Through Activating GATA Binding Protein 4 Signaling.
Article in MedComm, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- G6PC Downregulation Promotes Renal Calcium Oxalate Stone Formation via Lactate-Induced SNAIL1 K206 Lactylation and Epithelial-Mesenchymal Transition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- c-Myc: an emerging participant in heart failure.Frontiers in cardiovascular medicine · 2026Review
- Lactylation Modification: From Basic Biological Process to Clinical Cardiovascular Diseases.Research (Washington, D.C.) · 2026Review
- Histone H3 Lysine 18 Lactylation Promotes Cardiac Hypertrophy Through Activating GATA Binding Protein 4 Signaling.MedComm · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
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Abstract
Histone lactylation, particularly histone H3 lysine 18 lactylation (H3K18la), modulates gene expression profile in diverse cellular processes, which has emerged as a critical factor in cardiovascular disease pathogenesis. However, its specific role in cardiac hypertrophy remains unclear. This study investigates the mechanism of H3K18la in promoting cardiac hypertrophy using transverse aortic constriction-induced mice model and a phenylephrine-induced hypertrophic cardiomyocyte model. We found that elevated levels of Pan-Kla and H3K18la were detected in hypertrophic left ventricular tissues and cardiomyocytes, accompanied by increased heart and left ventricle weights, enlarged cardiomyocyte cross-sectional areas and heightened expression of ANP, BNP, and β-MHC. Clinical observations revealed a positive correlation between serum lactate levels and hypertrophic cardiomyopathy in patients. Furthermore, inhibition of lactylation reversed these effects, suggesting a direct role of H3K18la in hypertrophic gene expression. Mechanistically, H3K18la was found to interact with GATA4, enhancing its transcriptional activity as demonstrated by increased ANP promoter activity. Moreover, suppression of GATA4 mitigated the hypertrophic response, highlighting its crucial role downstream of H3K18la. Our findings identify H3K18la lactylation as a novel epigenetic mechanism driving cardiac hypertrophy through GATA4 activation. This implicates potential therapeutic targets for hypertrophic heart diseases.
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