Research Paper Volume 13, Issue 2 pp 2982—3009
Excessive fibroblast growth factor 23 promotes renal fibrosis in mice with type 2 cardiorenal syndrome
Figure 2. Upregulation of FGF23 in the heart and kidneys and activation of fibrosis-related signaling pathways in the kidneys by cardiorenal syndrome (CRS) at 12 weeks after induction of MI. (A) Serum FGF23 level measured by ELISA. ***P < 0.001 vs. sham mice, n = 12 per group. (B) Immunohistochemical staining shows enhanced FGF23 Protein expression in the myocardium and renal tubules of CRS mice compared with sham mice. (C) Western blot of FGF23, FGFR4 and Klotho in the kidneys of Sham and CRS mice. (D) Semi-quantitative assessment of FGF23, FGFR4 and Klotho. **P < 0.01, ***P < 0.001 vs. sham mice, n = 6 per group. (E) Western blot of collagen I, vimentin and TGF-β. **P < 0.01, ***P < 0.001 vs. sham mice, n = 6 per group. (F) Western blotting reveals significant upregulation of p-GSK-3β and active-β-catenin protein expression in the kidneys of CRS mice. ***P < 0.001 vs. sham mice, n = 6 per group. Data are means ± SE.