fig2

Figure 2. Histone lactylation links metabolic adaptation to HCC progression in the tumor microenvironment (TME). In the HCC-TME, contextual cues (hypoxia, aberrant glycolysis gene expression, high energy demand) drive enhanced glycolysis (the Warburg effect): glucose is metabolized to pyruvate, which is preferentially converted to pyruvate, leading to lactate accumulation. This metabolic adaptation enables epigenetic modification via histone lactylation, which triggers key pro-tumor processes that converge to accelerate HCC progression, establishing a feedforward loop between metabolic adaptation and epigenetic regulation in the HCC-TME. HCC: Hepatocellular carcinoma.