ArticleClinical and experimental nephrology2022
Circ_0000064 knockdown attenuates high glucose-induced proliferation, inflammation and extracellular matrix deposition of mesangial cells through miR-424-5p-mediated WNT2B inhibition in cell models of diabetic nephropathy.
Article in Clinical and experimental nephrology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Circular RNAs in diabetes mellitus and its complications: a systematic review and in silico analyses.Endocrine connections · 2025Article
- MiR-192-5p targets cell cycle regulation in diabetic kidney disease via cyclin-dependent kinase inhibitor 3.Non-coding RNA research · 2025Article
- Circular RNAs in Organ Fibrosis.Advances in experimental medicine and biology · 2025Review
- A predicted epithelial-to-mesenchymal transition-associated mRNA/miRNA axis contributes to the progression of diabetic liver disease.Scientific reports · 2024Article
- Circular RNA KIAA0564 Serves as a Competitive Endogenous RNA for MicroRNA-424-5p, Mediating the Expression of Lysine Demethylase 4a, Thereby Facilitating Intervertebral Disc Degeneration.Applied biochemistry and biotechnology · 2024Article
- Hsa_circ_0008360 promotes high glucose-induced damage in HK-2 cells via miR-346/WNT2B axis.Journal of endocrinological investigation · 2024Article
- Circular RNAs and the regulation of gene expression in diabetic nephropathy (Review).International journal of molecular medicine · 2024Article
- CircRNAs: versatile players and new targets in organ fibrosis.Cell communication and signaling : CCS · 2023Review
- Epigenetic modification in diabetic kidney disease.Frontiers in endocrinology · 2023Review
Corrections and comments
- Retracted
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCircular RNA (circRNA) is widely shown to be associated with the development of diabetic nephropathy (DN). Our study aimed to further explore the role of circ_0000064 and provide a new mechanism for its action in DN.
methodsCell models of DN in vitro were constructed by treating human renal mesangial cells (HRMCs) with high glucose (HG). The expression of circ_0000064, microRNA-424-5p (miR-424-5p) and Wnt family member 2B (WNT2B) mRNA was detected by quantitative real-time PCR (qPCR). Cell proliferation was assessed by CCK-8 assay and EdU assay. Cell cycle was characterized by DNA content using flow cytometry. The releases of pro-inflammatory factors were checked using commercial ELISA kits. The expression of cell cycle- and fibrosis-associated proteins was detected by western blot. The interplays between miR-424-5p and circ_0000064 or WNT2B were verified by dual-luciferase reporter assay and RIP assay.
resultsCirc_0000064 and WNT2B were upregulated, while miR-424-5p was downregulated in HG-treated HRMCs. Circ_0000064 knockdown largely attenuated HG-induced proliferation, inflammatory responses and extracellular matrix (ECM) accumulation in HRMCs, and miR-424-5p deficiency reversed the role of circ_0000064 knockdown. MiR-424-5p was a target of circ_0000064, and miR-424-5p directly bound to WNT2B. MiR-424-5p restoration alleviated HG-induced proliferation, inflammatory responses and ECM accumulation in HRMCs, and WNT2B overexpression partially abolished the effects of miR-424-5p.
conclusionCirc_0000064 knockdown ameliorated HG-induced HRMC dysfunctions through miR-424-5p enrichment-mediated WNT2B inhibition, hinting that circ_0000064 contributed to DN development.
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