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 3. Cardiac overexpression of FGF23 enhanced cardiac fibrosis and renal dysfunction. (A) The results of frozen sections showed that adeno-associated virus (AAV) carrying the FGF23 plasmid or negative control (NC) successfully infected the heart. (B) Confirmation of FGF23 overexpression in mouse hearts. Myocardial FGF23 mRNA was measured by routine and real-time PCR 4 weeks later. ***P < 0.001. NS, no statistical significance. n = 4-14 per group. (C) Expression of FGF23 mRNA was not detected in the kidneys. (D) Left ventricular ejection fraction (LVEF) showed no statistical significance between the groups. Serum creatinine (E) and serum phosphorus (F) levels were measured by ELISA. **P < 0.01, ***P < 0.001. NS, no statistical significance, n = 4-8 per group. (G) Routine PCR and quantitative real-time PCR for Klotho mRNA in the kidneys. **P < 0.01 vs. sham group, n = 6 per group, respectively. (H) Western blot of FGF23, collagen I and Klotho in the heart and kidneys. **P < 0.01, ***P < 0.001 vs. sham group, n = 4 per group. (I) Serum FGF23 was measured by ELISA. ***P < 0.001. n = 8 per group. (J) Immunohistochemical detection of FGF23 expression in the heart and kidneys of mice with or without cardiorenal syndrome and injection of AAV-NC or AAV-FGF23. Data are means ± SE.