ReviewFrontiers in pharmacology2026
Lactylation in liver fibrosis: from molecular mechanisms to targeted therapeutic strategies.
Review in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
4 authors.
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Abstract
Metabolic reprogramming and epigenetic remodeling of hepatic stellate cells (HSCs) represent central driving events in liver fibrosis. Lactylation, a lactate-mediated post-translational modification (PTM), is proposed to converge on histone H3 lysine 18 lactylation (H3K18La) through the HK2-KAT8 positive feedback loop, the IGF2BP2-N6-methyladenosine (m6A)-aldolase A (ALDOA) cascade, and the HKDC1-ORMDL3 pathway, potentially driving pro-fibrotic transcriptional programs in a synergistic manner. H3K18La does not operate in isolation; its site-specific competition with acetylation, cascade amplification with m6A methylation, cooperation with G9a/DNMT1-mediated methylation, and antagonism with ubiquitination form a PTM interaction network. Therapeutically, interventions targeting lactate-metabolizing enzymes (HK2, LDH), lactylation writers (KAT8), and specific lactylation sites (PGK1-K353 interfering peptides) have demonstrated anti-fibrotic potential in preclinical models. Natural products including curcumol, limonin, and salidroside exhibit multi-target regulatory advantages. Muscle-derived SORBS3 lactylation-mediated trans-organ signaling and lactylation gene-based molecular subtyping expand the systemic dimensions of lactylation. This narrative review proposes a working hypothesis positioning H3K18La as a metabolic-epigenetic convergence node and outlines future directions including site-specific interventions, cell type-resolved lactylomics, and molecular subtyping-driven clinical trials, providing an integrated framework from basic research to translational applications for liver fibrosis.
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