Year: 2026
Type: article
Abstract: Metabolic associated steatohepatitis (MASH) is a chronic liver disease characterized pathologically by hepatic steatosis, inflammatory infiltration, and progressive fibrosis. In recent years, lactate-mediated protein lactylation has been revealed as a key bridge linking cellular metabolism to epigenetic regulation. This review systematically summarizes the molecular mechanisms of lactylation, with a focus on its specific pathway role in the pathogenesis of MASH. Protein lactylation may promote lipid accumulation by regulating the activity of key enzymes involved in lipid metabolism, such as fatty acid synthase, within hepatocytes and sites such as histone H3 lysine 18 lactylation (H3K18la), as well as signaling proteins like M2-type pyruvate kinase; and they drive extracellular matrix deposition and fibrosis progression by regulating H3K18la-SRY-related high mobility group box transcription factor 9-mediated activation of hepatic stellate cells. Additionally, it aims to elucidate the precise regulatory networks through which lactylation influences the core pathological processes of MASH, providing a theoretical foundation for the development of innovative therapeutic strategies that target protein lactylation.
Source: PubMed Central
Language: Chinese
Subfield: Hepatology
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W7225308251