ArticleScientific reports2025
MiR-203 improved renal cell injury in diabetic nephropathy by targeting SOCS6/SOCS7 and inhibiting JAK/STAT pathway activation.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Sex-Specific sRNA Signatures in Rat Liver Reveal Divergent Alterations Following Perinatal Exposure to Glyphosate and Its Mixture with 2,4-D and Dicamba.International journal of molecular sciences · 2026Article
- Review
- SOCS1 Mimetic Peptide Enhances Empagliflozin Improvement on Kidney Damage in the Type 2 Diabetes Mouse Model BTBR ob/ob.International journal of molecular sciences · 2026Article
- Association of Janus kinase 1 and 2 expression with clinical indices in diabetic kidney disease.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2026Article
- MiR-216a-5p protects against high glucose-induced HMC injury by targeting the HMGB1/RAGE signaling pathway.Frontiers in endocrinology · 2025Article
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Authors and funding
6 authors.
Funding
Abstract
This study investigates the role of miR-203 in regulating renal cell injury in diabetic nephropathy by targeting the suppressor of cytokine signaling (SOCS) proteins SOCS6 and SOCS7. Using NRK cells, we assessed apoptosis through flow cytometry and TUNEL assays, while real-time quantitative PCR (RT-PCR) quantified miRNA and mRNA expressions. Cell viability was measured using the CCK-8 assay, and cytokine levels were determined through ELISA. We also evaluated reactive oxygen species (ROS) and malondialdehyde (MDA) levels with specific assay kits. The dual luciferase assay confirmed the interaction of miR-203 with SOCS6 and SOCS7. Western blotting analyzed the protein levels of key signaling molecules including JAK1, p-JAK1, JAK2, p-JAK2, STAT3, and p-STAT3.Our findings revealed that high glucose (HG) treatment reduced miR-203 levels, leading to decreased NRK cell proliferation, increased cytokine concentrations (TNF-α, IL-1β, IL-4, IL-6), heightened ROS and MDA levels, and increased cell apoptosis. Notably, miR-203 mimics counteracted HG's detrimental effects, while miR-203 inhibitors exacerbated them. Mechanistically, miR-203 directly decreased SOCS6 and SOCS7 expression, thereby inhibiting JAK/STAT3 signaling. Thus, miR-203 provides protective effects against renal cell injury by modulating SOCS and their associated pathways.
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