Metabolic dysfunction-associated fatty liver disease （MAFLD） is a chronic liver disease with a persistently high prevalence rate worldwide. Its pathogenesis involves metabolic disorders in multiple systems， and there is still a lack of a complete theoretical regulatory framework. Lactate was once regarded as a terminal metabolic waste product of the glycolytic pathway； however， studies in recent years have been exploring its biological functions as a key signaling molecule， and the close association between dysregulated lactate metabolism and the development and progression of MAFLD has gradually become a research hotspot in the field of metabolic liver diseases. This article systematically introduces the core pathways and regulatory patterns of lactate metabolism， elaborates on the overall functional characteristics of lactate in the development and progression of MAFLD， and reviews the molecular mechanisms by which lactate mediates hepatic lipid metabolism disorders and drives inflammatory cascades through epigenetic regulatory mechanisms such as protein lactylation. In addition， it briefly describes the potential effect of lactate in modulating liver metabolic homeostasis via the gut-liver axis and summarizes the latest research advances in lactate metabolism and MAFLD. This article highlights that targeting lactate metabolic pathways is a critical entry point for deepening the understanding of the pathophysiological mechanisms of MAFLD， and it points out that non-canonical regulatory modes represented by lactylation are key breakthrough directions for future research. It also proposes that developing early diagnostic biomarkers and intervention targets for MAFLD based on the lactate metabolic network holds important theoretical value and clinical translation potential.