ArticleToxicological sciences : an official journal of the Society of Toxicology2016
MiR-17 Downregulation by High Glucose Stabilizes Thioredoxin-Interacting Protein and Removes Thioredoxin Inhibition on ASK1 Leading to Apoptosis.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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38 citing papers in PubMed.
- Research advances on the impact of gestational diabetes mellitus on offspring neurodevelopment.Diabetology & metabolic syndrome · 2026Review
- The Unfolded Protein Response-Novel Mechanisms, Challenges, and Key Considerations for Therapeutic Intervention.Cancers · 2025Review
- Maternal plasma microRNAs as potential biomarkers for triaging pregnancies of unknown location and ectopic pregnancy diagnosis.Non-coding RNA research · 2025Article
- Review
- Diagnostic Value of Serum miR-17-5p in Type 2 Diabetes Mellitus and Its Predictive Value for Chronic Complications.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- Article
- miR-17-5p Promotes Glucose Uptake of HTR8/SVneo Trophoblast Cells by Inhibiting TXNIP/NLRP3 Inflammasome Pathway.Diabetes, metabolic syndrome and obesity : targets and therapy · 2022Article
- Dietary berberine alleviates high carbohydrate diet-induced intestinal damages and improves lipid metabolism in largemouth bass (Frontiers in nutrition · 2022Article
- Thioredoxin-interacting protein in diabetic retinal neurodegeneration: A novel potential therapeutic target for diabetic retinopathy.Frontiers in neuroscience · 2022Review
- Investigation of the role of the miR17-92 cluster in BMP9-induced osteoblast lineage commitment.Journal of orthopaedic surgery and research · 2021Article
- Xenograft Zebrafish Models for the Development of Novel Anti-Hepatocellular Carcinoma Molecules.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Micro RNAs in Regulation of Cellular Redox Homeostasis.International journal of molecular sciences · 2021Review
- The Emerging Role of TXNIP in Ischemic and Cardiovascular Diseases; A Novel Marker and Therapeutic Target.International journal of molecular sciences · 2021Review
- Crosstalk Between ER Stress, Autophagy and Inflammation.Frontiers in medicine · 2021Review
- MiR-17-5p Inhibits TXNIP/NLRP3 Inflammasome Pathway and Suppresses Pancreatic β-Cell Pyroptosis in Diabetic Mice.Frontiers in cardiovascular medicine · 2021Article
- Deficiency of the oxidative stress-responsive kinase p70S6K1 restores autophagy and ameliorates neural tube defects in diabetic embryopathy.American journal of obstetrics and gynecology · 2020Article
- GW0742 activates miR-17-5p and inhibits TXNIP/NLRP3-mediated inflammation after hypoxic-ischaemic injury in rats and in PC12 cells.Journal of cellular and molecular medicine · 2020Article
- Review
- Epigenetics and Mechanobiology in Heart Development and Congenital Heart Disease.Diseases (Basel, Switzerland) · 2019Review
- Modulating Expression of Thioredoxin Interacting Protein (TXNIP) Prevents Secondary Damage and Preserves Visual Function in a Mouse Model of Ischemia/Reperfusion.International journal of molecular sciences · 2019Article
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3 authors.
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Abstract
Pregestational diabetes significantly increases the risk of neural tube defects (NTDs). Maternal diabetes activates an Apoptosis Signal-regulating Kinase 1 (ASK1)-initiated pathway, which triggers neural stem cell apoptosis of the developing neuroepithelium leading to NTD formation. How high glucose of diabetes activates ASK1 is still unclear. In this study, we investigated the mechanism underlying high glucose-induced ASK1 activation. High glucose suppressed miR-17 expression, which led to an increase in its target gene Txnip (Thioredoxin-interacting protein). High glucose-increased Txnip enhanced its binding to the ASK1 inhibitor, thioredoxin (Trx), and thereby sequestered Trx from the Trx-ASK1 complex. High glucose-induced ASK1 activation and consequent apoptosis were abrogated by either the miR-17 mimic or Txnip siRNA knockdown. In contrast, the miR-17 inhibitor or Txnip ectopic overexpression mimicked the stimulative effect of high glucose on ASK1 and apoptosis. Thus, our study demonstrated that miR-17 repression mediates the pro-apoptotic effect of high glucose, and revealed a new mechanism underlying ASK1 activation, in which decreased miR-17 removes Trx inhibition on ASK1 through Txnip.
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