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CCN2/connective tissue growth factor (CTGF) potentially serves as a therapeutic target for chronic kidney disease. Here we investigated CCN2 module-4, encoded by  Ccn2  exon 5, through the generation of  Ccn2  exon 5 knockout mice ( Ex5 −/−mice). To investigate renal fibrosis pathogenesis,  Ex5 −/−mice were employed to model unilateral ureteral obstruction (UUO), unilateral ischemic-reperfusion injury (UIRI), and 5/6 nephrectomy. Interstitial fibrosis was significantly attenuated in the  Ex5 −/−mice in the three models. Furthermore, phosphorylated focal adhesion kinase (FAK) levels in tubular epithelial cells were significantly lower in the kidneys of the UUO- and UIRI- Ex5 −/−mice than those of the  Ex5 +/+mice. Moreover, CCN2 module 4-mediated renal tubule FAK and promoted fibrosis. These findings indicate that CCN2 module-4–FAK pathway components will serve as therapeutic targets for effectively attenuating renal fibrosis.

molecular and cellular biology

Module 4-Deficient CCN2/Connective Tissue Growth Factor Attenuates the Progression of Renal Fibrosis via Suppression of Focal Adhesion Kinase Phosphorylation in Tubular Epithelial Cells