Open AccessCircular RNA circEIF4G2 aggravates renal fibrosis in diabetic nephropathy by sponging miR‐218
Author(s) -
Xu Bojin,
Wang Qianqian,
Li Wenyi,
Xia Lili,
Ge Xiaoxu,
Shen Lisha,
Cang Zhen,
Peng Wenfang,
Shao Kan,
Huang Shan
Publication year - 2022
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.16129
Subject(s) - gene knockdown , fibronectin , diabetic nephropathy , circular rna , fibrosis , cancer research , microbiology and biotechnology , downregulation and upregulation , kidney , cell , chemistry , biology , cell culture , endocrinology , medicine , gene , biochemistry , genetics
Circular RNAs play essential roles in the development of various human diseases. However, how circRNAs are involved in diabetic nephropathy (DN) are not fully understood. Our study aimed to investigate the effects of circRNA circEIF4G2 on DN. Experiments were performed in the db/db mouse model of type 2 diabetes and NRK‐52E cells. We found that circEIF4G2 was significantly up‐regulated in the kidneys of db/db mice and NRK‐52E cells stimulated by high glucose. circEIF4G2 knockdown inhibited the expressions of TGF‐β1, Collagen I and Fibronectin in high glucose‐stimulated NRK‐52E cells, which could be rescued by miR‐218 inhibitor. Knockdown of SERBP1 reduced the expression of TGF‐β1, Collagen I and Fibronectin in HG‐stimulated NRK‐52E cells. In summary, our findings suggested that circEIF4G2 promotes renal tubular epithelial cell fibrosis via the miR‐218/SERBP1 pathway, presenting a novel insight for DN treatment.