ArticleBiochemical genetics2022
LncRNA NEAT2 Modulates Pyroptosis of Renal Tubular Cells Induced by High Glucose in Diabetic Nephropathy (DN) by via miR-206 Regulation.
Article in Biochemical genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- Advances in understanding the NLRP3 inflammasome‑mediated mechanisms and therapeutic targets in diabetic nephropathy (Review).International journal of molecular medicine · 2026Review
- Roles of microRNAs in cardiorenal syndrome.Molecular and cellular biochemistry · 2025Review
- Regulation of pyroptosis in diabetic nephropathy by long non-coding and circular RNAs.Clinical and experimental medicine · 2025Review
- Uncovering the mechanism of Huangkui capsule in the treatment of diabetic kidney disease based on network pharmacology and experimental validation.Scientific reports · 2025Article
- Targeting programmed cell death in diabetic kidney disease: from molecular mechanisms to pharmacotherapy.Molecular medicine (Cambridge, Mass.) · 2024Review
- LncRNA KIFAP3-5:1 inhibits epithelial-mesenchymal transition of renal tubular cell through PRRX1 in diabetic nephropathy.Cell biology and toxicology · 2024Article
- GLP-1RAs inhibit the activation of the NLRP3 inflammasome signaling pathway to regulate mouse renal podocyte pyroptosis.Acta diabetologica · 2024Article
- Autophagy, Pyroptosis and Ferroptosis are Rising Stars in the Pathogenesis of Diabetic Nephropathy.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Review
- The Role of Pyroptosis in the Pathogenesis of Kidney Diseases.Kidney diseases (Basel, Switzerland) · 2023Review
- Natural products in attenuating renal inflammationFrontiers in immunology · 2023Review
- Connexins and Glucose Metabolism in Cancer.International journal of molecular sciences · 2022Review
- Potential therapeutic role of pyroptosis mediated by the NLRP3 inflammasome in type 2 diabetes and its complications.Frontiers in endocrinology · 2022Review
- NLRP3-mediated pyroptosis in diabetic nephropathy.Frontiers in pharmacology · 2022Review
- Long Non-Coding RNAs in the Pathogenesis of Diabetic Kidney Disease.Frontiers in cell and developmental biology · 2022Review
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Patients suffering from terminal-stage diabetic nephropathy (DN) are commonly diagnosed with kidney failure. The condition of DN patients gets generally improved by long-chain noncoding RNA (LncRNA) since it regulates microRNA (miR). The current study analyzes the role played by NEAT2/miR-206 upon cell death of renal tubular epithelial cells (RTECs), high glucose (HG)-induced inflammation and oxidative stress in diabetic nephropathy (DN). The researcher used high glucose (HG) to treat HK-2 cells in in vitro conditions to establish the DN cell model. qRT-PCR was used to confirm the transfection effect whereas the researcher also tested NEAT2, nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain containing (NLRP3), caspase-1, interleukin IL-1β, gasdermin D (GSMDD)-N, and miR-206. To analyze the proteins in caspase-1, IL-1β, GSMDD-N, and NLRP3, Western blot technique was performed. The technique is also used to observe the pyroptosis. To identify TNF-α, IL-6, MCP-9, NEAT2, miR-206, and NLRP3, dual-luciferase reporter assay was conducted through ELISA kit to emphasize the correlation that exists among the above-mentioned factors. NEAT2 has been confirmed to have bound with miR-206 through double luciferase report experiments as well as RNA immunoprecipitation (RIP). NEAT2, present in HK-2 cells, was induced by HG. So, if NEAT2 is knocked down, it would mitigate TNF-α, IL-6, and MCP-9 as well. Among the HK-2 cells intervened with HG, the overexpressed miR-206 that was transfected into cells was in alignment with the modifications introduced in inflammatory factors and cytokines after NEAT2 is knocked down. The current study concludes that if NEAT2 is upregulated, it has the potential to retreat the inhibition of miR-206 on inflammatory response as well pyroptosis. Further, by targeting miR-206, NEAT2 has the potential to enhance HG-induced HK-2 pyroptosis. This miR-206 is predicted to be a latent target in the clinical treatment of DN.
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