However, the excessive accumulation of M2 macrophages in lung tissue leads to heightened expression of pro-fibrotic factors like TGF-β, vascular endothelial growth factors (VEGF), platelet-derived growth factor (PDGF), and Th2 cytokines including IL-13 and IL-33, exacerbating pulmonary fibrosis development (Li et al., 2014; Zhang et al., 2022). This evidence concerns the gene VEGFA and pulmonary fibrosis.