FGF23 promotes renal interstitial fibrosis by activating β-catenin

Q. Zhu, D.-K. Zeng, F.-Q. Li

Department of Geriatrics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. lifaqi1280@163.com

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• Nephrology

OBJECTIVE: To investigate the role and mechanism of fibroblast growth factor 23 (FGF23) in renal interstitial fibrosis.

MATERIALS AND METHODS: Rat renal tubular epithelial cell line (NRK-52E) was selected for in vitro experiments. Effect of FGF23 on extracellular matrix was observed. High expression of FGF23 was induced by injecting the plasmid into the caudal vein. The model of unilateral ureteral obstruction (UUO) was established for in vivo experiments.

RESULTS: FGF23 increased the expression of extracellular matrix proteins FN, α-SMA and Type 1 collagen of NRK-52E induced by TGFβ1, while FGF23 increased the expression of p-β-catenin 675. In UUO model mice, fibrosis in the FGF23 high expression group increased significantly compared to that of the control group. Meanwhile, β-catenin signal was activated.

CONCLUSIONS: FGF23 can promote the deposition of extracellular matrix of NRK-52E induced by TGFβ1 in vitro. It aggravated the degree of renal interstitial fibrosis in UUO model, which is related to the activation of β-catenin signaling pathway.

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