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<p>Metabolic dysfunction-associated steatotic liver disease (MASLD) is a prevalent chronic liver disorder with limited therapeutic options. While its pathogenesis is complex, the underlying molecular drivers remain incompletely understood. Recently, protein lactylation, a novel lactate-derived post-translational modification (PTM), has emerged as a key regulator linking metabolic reprogramming to cellular function. This review elucidates the pivotal roles of protein lactylation throughout the progression of MASLD, from simple steatosis to metabolic dysfunction-associated steatohepatitis (MASH) and hepatocellular carcinoma, establishing a conceptual framework centered on the “lactate-lactylation-gene expression” axis and examining its dysregulation across hepatocytes, hepatic stellate cells, and immune cells throughout MASLD. Furthermore, we discuss emerging therapeutic strategies targeting the axis, aiming to provide a theoretical foundation for the development of precision medicine for MASLD.</p>

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Protein lactylation in metabolic dysfunction-associated steatotic liver disease: a mechanistic review

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月9日

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  • Huilin Chen,
  • Yuntao Ye,
  • Tianmu He,
  • Bo Li,
  • Qiang Wang

摘要

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a prevalent chronic liver disorder with limited therapeutic options. While its pathogenesis is complex, the underlying molecular drivers remain incompletely understood. Recently, protein lactylation, a novel lactate-derived post-translational modification (PTM), has emerged as a key regulator linking metabolic reprogramming to cellular function. This review elucidates the pivotal roles of protein lactylation throughout the progression of MASLD, from simple steatosis to metabolic dysfunction-associated steatohepatitis (MASH) and hepatocellular carcinoma, establishing a conceptual framework centered on the “lactate-lactylation-gene expression” axis and examining its dysregulation across hepatocytes, hepatic stellate cells, and immune cells throughout MASLD. Furthermore, we discuss emerging therapeutic strategies targeting the axis, aiming to provide a theoretical foundation for the development of precision medicine for MASLD.