participates in renal fibrosis -mediated epithelial-mesenchymal transition of proximal tubular epithelial cells.

BACKGROUND

Fos-related antigen 2 () plays a facilitative role in fibrotic disease; however, its role in renal fibrosis remains unclear. This study aimed to clarify the role and underlying mechanisms of in renal fibrosis.

METHODS

Upregulated genes in unilateral ureteral obstruction (UUO)-injured kidneys were screened in Gene Expression Omnibus (GEO) databases, and overlapping genes were identified using Venn diagram software. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed for these genes. The UUO-induced mouse model and transforming growth factor-β1 (TGF-β1)-induced cell model were used for the and studies.

RESULTS

A total of 43 commonly upregulated genes were identified. GO and KEGG pathway analyses indicated that may be involved in fibrosis. Furthermore, was confirmed to be upregulated in UUO-injured kidneys and TGF-β1-induced cells. Knockdown of ameliorated interstitial fibrosis, extracellular matrix deposition, and epithelial-mesenchymal transition the downregulation of fibronectin, α-smooth muscle actin (α-SMA), collagen type I ( and ), and and upregulation of . Bioinformatics analysis revealed that serum/glucocorticoid regulated kinase 1 () may be regulated by and involved in renal fibrosis. Further experiments confirmed that TGF-β1 enhanced expression and transcription, which were reversed by silencing. Moreover, was bound to the promoter, and overexpression reversed the effects of silencing in TGF-β1-induced cells.

CONCLUSION

plays an essential role in promoting renal fibrosis in an -dependent manner, and targeting the / signaling axis may offer a potential strategy for the treatment of renal fibrosis.