Research Paper Volume 13, Issue 2 pp 2982—3009

Excessive fibroblast growth factor 23 promotes renal fibrosis in mice with type 2 cardiorenal syndrome

FGF23 overexpression further enhanced cardiac and renal fibrosis, and promoted activation of fibrosis-related signaling pathways in the kidneys of mice with cardiorenal syndrome (CRS). (A) Representative photomicrographs of myocardial and renal fibrosis detected by Masson’s trichrome stain in sham, AAV-NC and AAV-FGF23 mice or CRS mice injected with AAV-NC or AAV-FGF23, or treated with PD173074 or DMSO. (B–D) Semi-quantitative assessment of myocardial, renal glomerular and interstitial fibrosis. (B–D) **P ***P E) Western blot of collagen I, vimentin and TGF-β. (F) Western blot of p-GSK-3β and active-β-catenin. For (E and F), *P **P ***P

Figure 4. FGF23 overexpression further enhanced cardiac and renal fibrosis, and promoted activation of fibrosis-related signaling pathways in the kidneys of mice with cardiorenal syndrome (CRS). (A) Representative photomicrographs of myocardial and renal fibrosis detected by Masson’s trichrome stain in sham, AAV-NC and AAV-FGF23 mice or CRS mice injected with AAV-NC or AAV-FGF23, or treated with PD173074 or DMSO. (BD) Semi-quantitative assessment of myocardial, renal glomerular and interstitial fibrosis. (BD) **P < 0.01, ***P < 0.001. n = 5 per group. (E) Western blot of collagen I, vimentin and TGF-β. (F) Western blot of p-GSK-3β and active-β-catenin. For (E and F), *P < 0.05. **P < 0.01, ***P < 0.001. NS, no statistical significance, n = 3 per group. Data are means ± SE.