ArticleAnnals of translational medicine2021
LncRNA KCNQ1OT1 promoted hepatitis C virus-induced pyroptosis of β-cell through mediating the miR-223-3p/NLRP3 axis.
Article in Annals of translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Macrophage ACAT1 Aggravates Alcohol-Associated Liver Disease by Inducing Mitochondrial Damage and NLRP3 Activation.Journal of gastroenterology and hepatology · 2026Article
- The Association Between miRNA-223-3p Levels and Pain Severity in Fibromyalgia Syndrome: A Molecular Approach.International journal of molecular sciences · 2025Article
- LncRNA-Gm17586 inhibits S.typhimurium mediated pyroptosis by promoting NLRP3 and Tnip1 binding.Scientific reports · 2025Article
- Study and validation on mitochondrial and immune-related hub genes in gestational diabetes mellitus based on bioinformatics.Frontiers in endocrinology · 2025Article
- Silencing lncRNA KCNQ1OT1 reduced hepatic ischemia reperfusion injury-induced pyroptosis by regulating miR-142a-3p/HMGB1 axis.Molecular and cellular biochemistry · 2023Article
- T2DB: A Web Database for Long Non-Coding RNA Genes in Type II Diabetes.Non-coding RNA · 2023Article
- LncRNA AC040162.3 Promotes HCV-Induced T2DM Deterioration through the miRNA-223-3p/NLRP3 Molecular Axis.Analytical cellular pathology (Amsterdam) · 2023Article
- Non-coding RNAs in diabetes mellitus and diabetic cardiovascular disease.Frontiers in endocrinology · 2022Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundType 2 diabetes is a well described extra-hepatic manifestation of hepatitis C virus (HCV) infection. This study aimed to explore the potential mechanism of KCNQ1 overlapping transcript 1 (KCNQ1OT1) in type 2 diabetes mellitus (T2DM) caused by HCV infection.
methodsMin6 cells were infected with HCV to establish a vitro model, and the HCV copy number was detected by real-time quantitative PCR (RT-qPCR). The mRNA and protein expressions of IL-1β, IL-18, NLRP3, caspase-1, and GSDMD were analyzed by RT-qPCR and Western blot. Flow cytometry and TUNEL assay were used to evaluate the pyroptosis of cells and enzyme-linked immunosorbent assay (ELISA) detected the secretion of insulin. A dual luciferase reporter gene assay then verified the targeting relationship of KCNQ1OT1, miRNA-223-3p, and NLRP3.
resultsKCNQ1OT1 was highly expressed in HCV-infected T2DM patients and HCV-infected β-cells. Silencing KCNQ1OT1 inhibited β-cell pyroptosis by regulating miR-223-3p/NLRP3, and inhibition of miR-223-3p or overexpression of NLRP3 reversed the pyroptosis by silencing KCNQ1OT1.
conclusionsOur findings indicate KCNQ1OT1 promotes HCV-infected β-cell pyroptosis through the miRNA-223-3p/NLRP3 axis, effecting the production of insulin and accelerating the occurrence and development of T2DM.Regulating KCNQ1OT1 and its target genes will help to better understand the pathogenesis of T2DM induced by HCV infection and provide new theoretical foundations and therapeutic targets.
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