ArticleDisease markers2022
circ_000166/miR-296 Aggravates the Process of Diabetic Renal Fibrosis by Regulating the SGLT2 Signaling Pathway in Renal Tubular Epithelial Cells.
Article in Disease markers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- MicroRNA Regulation in Kidney Interstitial Fibrosis.Epigenomes · 2026Review
- Circ_0039857: A Key Player in Combating Immune Disorders and Ferroptosis in High-Glucose-induced HK-2 Cells and Diabetic Kidney Disease Mice.Applied biochemistry and biotechnology · 2026Article
- CD248, targeted by veratramine and neobavaisoflavone, mediates pathological changes of renal tubular epithelial cells induced by high glucose.Hereditas · 2025Article
- Circular RNAs and the regulation of gene expression in diabetic nephropathy (Review).International journal of molecular medicine · 2024Article
- Epigenetic modification in diabetic kidney disease.Frontiers in endocrinology · 2023Review
- Upregulation of miR145 and miR126 in EVs from Renal Cells Undergoing EMT and Urine of Diabetic Nephropathy Patients.International journal of molecular sciences · 2022Article
- Review
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic renal fibrosis is a common cause of end-stage renal disease, and the circRNA-miRNA-mRNA network may play an important role in the progression of diabetic nephropathy- (DN-) induced renal fibrosis. In this study, the role of circ_000166/miR-296/SGLT2 in the process of DN-related renal fibrosis was studied by constructing an animal model of DN renal fibrosis via lentiviral transfection, plasmid transfection, and dual-luciferase reporting techniques. Compared with that of normal controls, the expression of circ_000166 in the kidney tissues of DN renal fibrosis mice substantially increased. Silencing circ_000166 could minimize kidney damage and decrease urine protein levels, thereby inhibiting the progression of renal fibrosis. Moreover, circ_000166 could act as the ceRNA of miR-296 and competitively bind to miR-296, leading to an increase in the expression of the SGLT2 gene regulated by miR-296. Through mutual verification via in vivo and in vitro experiments, miR-296 was overexpressed and SGLT2 was silenced. Results showed that DN renal fibrosis and cell apoptosis were considerably reduced. We postulate that circ_000166/miR-296/SGLT2 may become a new target in the progression of DN renal fibrosis, and the regulation of this pathway may be a promising strategy for clinical treatment of DN renal fibrosis.
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Registered trials
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