ArticleJournal of neuroinflammation2018
IRE1α inhibition decreased TXNIP/NLRP3 inflammasome activation through miR-17-5p after neonatal hypoxic-ischemic brain injury in rats.
Article in Journal of neuroinflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers.
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Who cites it
101 citing papers in PubMed, 198 citations in OpenAlex.
- Intranasal therapies for neonatal hypoxic-ischemic encephalopathy.Neural regeneration research · 2026Article
- Aldose reductase inhibition suppresses microglial endoplasmic reticulum stress and ferritinophagy in ischemic stroke.Acta pharmacologica Sinica · 2026Article
- Microplastics Exacerbate Cadmium-Induced Hepatotoxicity via the IRE1α/TXNIP/NLRP3 Axis-Driven Endoplasmic Reticulum Stress and Pyroptosis.Veterinary sciences · 2026Article
- Redox rewiring in glioblastoma: the thioredoxin system as a precision therapeutic target.Pharmacological reports : PR · 2026Review
- Non-Targeting shRNA-Encoded Plasmid DNA Enhances Protective Immunity Through RIDD-RIG-I Signaling Pathway in the Zika Virus Animal Model.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeting the UPR with Small Molecules: Emerging Strategies for Immune Regulation.Molecules (Basel, Switzerland) · 2026Review
- Thioredoxin-Binding protein 2 and apoptosis Signal-Regulating kinase 1: redox stress sensors and therapeutic targets in hepatocellular carcinoma.Medical oncology (Northwood, London, England) · 2026Review
- PKM2 preconditioning protects endothelial cells from pyroptosis and BBB disruption via NRF2/TRX/TXNIP signaling in neonatal hypoxic-ischemic brain injury.Journal of neuroinflammation · 2026Article
- Modified Xiaoyao San ameliorates LPS-induced depression-like behavior by inhibiting NLRP3-mediated microglial pyroptosis.Metabolic brain disease · 2025Article
- Microglial STING activation promotes neuroinflammation and pathological changes in experimental mice with intracerebral haemorrhage.Acta pharmacologica Sinica · 2025Article
- Tonabersat Inhibits Retinal Inflammation After Hypoxia-Ischemia in the Neonatal Rat.International journal of molecular sciences · 2025Article
- Targeting α‑Klotho Protein by Agmatine and Pioglitazone Is a New Avenue against Diabetic Nephropathy.ACS pharmacology & translational science · 2025Article
- NLRP3 inflammasome: a key player in neonatal brain injury.Clinical and experimental pediatrics · 2025Article
- Role of microRNA-498 and microRNA-410 in neonatal hypoxic-ischemic encephalopathy.Clinical and experimental pediatrics · 2025Article
- Astragaloside IV Alleviates Podocyte Injury in Diabetic Nephropathy through Regulating IRE-1α/NF-κ B/NLRP3 Pathway.Chinese journal of integrative medicine · 2025Article
- Exploring NLRP3 Inhibition as a Key Modulator in Neonatal Hypoxic-Ischemic Brain Injury.Neuromolecular medicine · 2025Review
- Targeting NLRP3 Inflammasomes: A Trojan Horse Strategy for Intervention in Neurological Disorders.Molecular neurobiology · 2025Review
- The antiarthritic effect of CBR-470-1 in hypoxic environment is to increase the level of NOD-like receptor family pyrin domain containing 3 ubiquitination by decreasing phosphoglycerate kinase 1 activity.Clinical and translational medicine · 2025Article
- Review
- Celastrol ameliorates hypoxic-ischemic brain injury in neonatal rats by reducing oxidative stress and inflammation.Pediatric research · 2024Article
41 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundThe endoplasmic reticulum (ER) is responsible for the control of correct protein folding and protein function which is crucial for cell survival. However, under pathological conditions, such as hypoxia-ischemia (HI), there is an accumulation of unfolded proteins thereby triggering the unfolded protein response (UPR) and causing ER stress which is associated with activation of several stress sensor signaling pathways, one of them being the inositol requiring enzyme-1 alpha (IRE1α) signaling pathway. The UPR is regarded as a potential contributor to neuronal cell death and inflammation after HI. In the present study, we sought to investigate whether microRNA-17 (miR-17), a potential IRE1α ribonuclease (RNase) substrate, arbitrates downregulation of thioredoxin-interacting protein (TXNIP) and consequent NLRP3 inflammasome activation in the immature brain after HI injury and whether inhibition of IRE1α may attenuate inflammation via miR-17/TXNIP regulation.
methodsPostnatal day 10 rat pups (n = 287) were subjected to unilateral carotid artery ligation followed by 2.5 h of hypoxia (8% O
resultsEndogenous phosphorylated IRE1α expression was significantly increased after HI. Intranasal administration of STF-083010 alleviated brain injury and improved neurological behavior. MiR-17-5p expression was reduced after HI, and this decrease was attenuated by STF-083010 treatment. MiR-17-5p mimic administration ameliorated TXNIP expression, NLRP3 inflammasome activation, caspase-1 cleavage, and IL-1β production, as well as brain infarct volume. Conversely, anti-miR-17-5p inhibitor reversed IRE1α inhibition-induced decrease in TXNIP expression and inflammasome activation, as well as exacerbated brain injury after HI.
conclusionsIRE1a-induced UPR pathway may contribute to inflammatory activation and brain injury following neonatal HI. IRE1a activation, through decay of miR-17-5p, elevated TXNIP expression to activate NLRP3 inflammasome and aggravated brain damage.
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