Fig 2: Targeting YAP/TAZ to relieve AT fibrosis in obese mice.a–e Yapf/fTazf/fAdipoqCreERT2 (YT-iAKO) or YT-FF mice were fed a HFD for 11 weeks followed by i.p. injection of 5 doses of tamoxifen (50 mg/kg) every day (n = 6). a Experimental scheme. b mRNA expression of fibrosis markers in scWAT from YT-FF or YT-iAKO mice (n = 6). c Representative scWAT sections with Picrosirius red staining of YT-FF or YT-iAKO mice. d, e Glucose tolerance test (GTT) (d) or insulin tolerance test (ITT) (e) of YT-FF (n = 6) or YT-iAKO (n = 7) mice. f–l Eight-week-old ob/ob mice were i.p. injected with Veh or verteporfin (VP) (25 mg/kg) for 5 doses every other day. f Experimental scheme. g mRNA expression of fibrosis markers and YAP target genes in scWAT of ob/ob mice (n = 6). h Immunoblot analysis (left) and quantification (right) of Col1a1 (n = 3 mice). i Representative sections of scWAT stained for Col1a1 (red) and nucleus (DAPI, blue). j Representative scWAT sections with Picrosirius red staining of ob/ob mice. k GTT (n = 6 mice). l ITT (n = 6 mice). Data are means ± SEM. Two-tailed unpaired Student’s t test in b, g, h; two-way ANOVA with Bonferroni’s multiple-comparisons test in d, e, k, l; *P < 0.05, **P < 0.01, ***P < 0.001. Exact P values are provided in a Source data file.

Fig 3: iCSFCs have fibroblast properties. (A) Gene expression of fibroblast cell markers was examined by RT-PCR. Most fibroblast genes were expressed in iCSFCs, with the exception of Acan, MMP13 and Sox6. GAPDH was used as an internal control. (B,C) Immunocytochemistry analysis of iCSFCs for fibroblast marker proteins. Immunostaining was used to indicate fibroblast markers (red) in CFF-3 cells (B) and iCSFCs (C), including ALCAM, Col1A1, HSP47 and S100A4. Cell nuclei were labeled with DAPI (Scale bars, 50 μm).

Fig 4: ELISA results of VTN and COL1A1 between VUR and non-VUR groups. (A) ELISA result of VTN between VUR and non-VUR groups. (B) ELISA result of COL1A1 between VUR and non-VUR groups. (C) Receiver operating curve analysis of VTN between VUR and non-VUR groups. n=25 for the VUR group and n=35 for the non-VUR group. ****P<0.0001. n.s., not significant; VUR, vesicoureteral reflux; COL1A1, α-1 type I collagen; VTN, vitronectin; AUC, area under curve.

Fig 5: Morphological changes and Western blotting, immunofluorescence and immunohistochemical analyses of the parietal peritoneum. (A) Masson’s trichrome staining (100× magnification; scale bar, 100 μm). (B) Western blotting of epithelial or mesenchymal markers. (C) Immunofluorescence staining for E-cadherin (green) and α-SMA (red) with nuclear counterstaining (DAPI; blue) in the parietal peritoneum (400× magnification; scale bar, 20 μm). Cells positive for both E-cadherin and α-SMA are indicated by arrows. (D) Immunohistochemical staining for COL1A1 or fibronectin (200× magnification; scale bar, 50 μm). (E) Immunohistochemical staining for TGF-β (100× magnification; scale bar, 50 μm). CTL, control; PF, mice intraperitoneally injected with 0.1% chlorhexidine gluconate; PF + SB, PF with SB525334 administration by oral gavage; α-SMA, α-smooth muscle actin; OD, optical density; COL1A1, collagen type 1 alpha 1; TGF-β, transforming growth factor-beta 1. Thickness of the peritoneal membrane is expressed as mean ± standard error (n = 5 for CTL group, n = 6 for PF group, n = 8 for PF + SB group). * p < 0.05, compared to the corresponding group.