ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
PFKM-Driven Lactate Overproduction Promotes Atrial Fibrillation via Triggering Cardiac Fibroblasts Histone Lactylation.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Glycolytic enolase 1-induced H4K12 lactylation activates quiescent breast cancer stem-like cells in triple-negative breast cancer.Signal transduction and targeted therapy · 2026Article
- A multivariable prediction model for left atrial appendage spontaneous echo contrast in patients with atrial fibrillation: development and external validation.BMC cardiovascular disorders · 2026Article
- Histone lactylation: a novel epigenetic bridge linking cellular metabolism to benign and malignant gynecological diseases.Clinical epigenetics · 2026Review
- Lactylation in cardiac repair: Nexus and therapeutic opportunity.Journal of molecular and cellular cardiology plus · 2026Review
- Inhibiting lactylation for efficient treatment of renal fibrosis through targeting nanomedicine of renal lactate accumulation in obstructed kidney.Journal of nanobiotechnology · 2026Article
- Lactylation in tissue fibrosis: epigenetic mechanisms, metabolic crosstalk, and therapeutic opportunities.Journal of translational medicine · 2026Review
- Lactylation: a metabolic-epigenetic bridge in diabetic kidney disease and a therapeutic target for TCM.Chinese medicine · 2026Review
- The glycolytic enzyme PFKM promotes renal fibrosis by activating the NF-κB pathway via lactate-mediated H3K18 lactylation.Cellular and molecular life sciences : CMLS · 2026Article
- lncRNA NEAT1 promotes the proliferation of hemangioma cells by transcriptionally activating β‑catenin via enhancing H3K18 lactylation.Molecular medicine reports · 2026Article
- Tubular NAT10 Promotes the Secretion of TGF-β and Lactate to Drive Fibroblast Activation in Diabetic Kidney Disease.International journal of biological sciences · 2026Article
- Hypoxia-driven crosstalk among cardiac fibroblasts, macrophages, and endothelial cells in cardiac fibrosis.Frontiers in cell and developmental biology · 2026Review
- Lactylation in urological malignancies: emerging mechanisms and therapeutic direction.Frontiers in cell and developmental biology · 2026Review
- Cardiac fibroblast heterogeneity in cardiac fibrosis implication for cell-type-specific treatment.Frontiers in physiology · 2026Review
- Mitochondrial regulation of lactylation in sepsis-induced cardiomyopathy.Critical care (London, England) · 2025Review
- Integrated Multilayer Omics Reveals the Underlying Mechanisms in Xylazine-Related Heart Injury in Rats.International journal of molecular sciences · 2025Article
- PFKM-Driven Lactate Overproduction Promotes Atrial Fibrillation via Triggering Cardiac Fibroblasts Histone Lactylation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Abstract
Increasing evidence has clarified that atrial fibrillation (AF) is associated with enhanced glycolysis, leading to lactate accumulation. However, whether glycolysis promotes AF remains unknown, as does whether histone lactylation plays a role in its pathogenesis. In the study, spontaneous AF mice are established to monitor AF susceptibility and atrial substrates at different ages (3, 5, 7 months), indicating that enhanced glycolysis acts as a promoter during AF development by inducing atrial fibrosis. The promoting effect of glycolysis on AF and the pivotal enzyme in driving glycolysis are confirmed by treatment with glycolysis inhibitor 2-deoxyglucose (2-DG) and adeno-associated virus-mediated atrial PFKM expression. Furthermore, lactate stimulates primary mouse cardiac fibroblast (CF) activation. Mechanistically, the observations indicated that atrial lactate accumulation promotes global lactylation and H3K18 lactylation in atrial fibroblasts. P300-mediated H3K18 lactylation up-regulates TGF-β1 transcription, leading to activation of CF, and thereby contributing to atrial fibrosis. The results reveal a novel role of the metabolic-epigenetic axis in AF pathogenesis, which raises the possibility of potential therapeutic strategies targeting AF.
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