In conclusion, the current study demonstrated that GAS5 overexpression restrained TGF-β1-induced pericyte–myofibroblast transformation and bleomycin-induced PF by reducing PDGFR α/β expression through interaction with KDM5B to promote H3K4me2/3 demethylation, suggesting a negative regulatory role of GAS5 in the etiology of IPF (Fig. 9). Here, TGFB1 is linked to idiopathic pulmonary fibrosis.