FIGURE 8.

Schematic representation of PCBP3-PFKFB3-dependent glycolysis and the inhibitory effect of anlotinib on this pathway. Lung injury induces PCBP3 expression, which results in an increase in PFKFB3 expression by promoting its translation, resulting in the augmentation of glycolysis in lung fibroblasts. Glycolytic reprogramming participates in myofibroblast activation and furthers lung fibrosis. The tyrosine kinase inhibitor anlotinib inhibits PFKFB3-driven glycolysis by decreasing the expression of PCBP3, thereby suppressing myofibroblast activation and inhibiting the exacerbation of lung fibrosis.