Fig. 8.

Fibroblast-specific deletion of WTAP attenuates bleomycin-induced pulmonary fibrosis. (A) Schematic illustration of fibroblast-specific WTAP conditional knockout (cKO) mice generated by crossing WTAP^fl/fl mice with Col1a2-Cre transgenic mice and subsequent induction of pulmonary fibrosis by bleomycin (BLM). (B) Increased KLF6 occupancy at the Wtap promoter in WTAP-deficient mice after bleomycin challenge. (C) Kaplan–Meier survival curves showing the survival rate of WTAP^fl/fl and WTAP-cKO mice following BLM treatment. (D-E) Pulmonary function assessment of lung static compliance (Cst) (D) and inspiratory capacity (IC) (E) in WTAP^fl/fl and WTAP-cKO mice on day 21 after BLM challenge. (n = 4 per group). (F) Quantification of hydroxyproline content in lung tissues from WTAP^fl/fl and WTAP-cKO mice treated with BLM (n = 6 per group). (G) Representative hematoxylin and eosin (H&E) staining of lung sections showing fibrotic progression in WTAP^fl/fl and WTAP-cKO mice on day 21 post-BLM. Scale bar, 100 μm. (H-I) Representative immunofluorescence staining of COL1A1 and α-SMA (ACTA2) and corresponding quantitative analysis of fluorescence intensity in WTAP^fl/fl and WTAP-cKO lungs after BLM exposure (n = 6 per group). Scale bar, 50 μm. Data are presented as mean ± s.e.m. Statistical significance was determined by unpaired two-tailed Student’s t-test or log-rank (Mantel–Cox) test for survival analysis. P < 0.05 was considered significant. *p < 0.05; **p < 0.01; ***p < 0.001 compared to the corresponding groups