ArticleJournal of cellular and molecular medicine2020
Inhibition of microglial receptor-interacting protein kinase 1 ameliorates neuroinflammation following cerebral ischaemic stroke.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 31 citations in OpenAlex.
- GFH312 Reduces Neuronal Death by Inhibiting RIPK1-Mediated Apoptosis and Necroptosis After Ischemic Stroke.CNS neuroscience & therapeutics · 2026Article
- Targeting Ferroptosis and Necroptosis to Treat Stroke.Neurochemical research · 2026Review
- Receptor-Interacting Protein Kinase 1 (RIPK1): A Potential Therapeutic Target in Ischemic Stroke.Molecular neurobiology · 2026Review
- Transcranial Ultrasound Stimulation Pulsed at 40 Hz Improves Cognition and Neuroinflammation in Female Mice with Alzheimer's Disease.Research (Washington, D.C.) · 2026Article
- Acute Administration of Edaravone Improves Cognitive Impairment in a Mouse Model of mPFC Ischemia: Crosstalk Between Necroptosis, Neuroinflammation, and Antioxidant Defense.Molecular neurobiology · 2025Article
- Microglia programmed cell death in neurodegenerative diseases and CNS injury.Apoptosis : an international journal on programmed cell death · 2025Review
- Shenmai Injection enhances short-term outcomes in ischemic stroke patients after thrombolysis via AMPKα1.Frontiers in pharmacology · 2025Article
- Ripks and Neuroinflammation.Molecular neurobiology · 2024Review
- Itaconate inhibits corticosterone-induced necroptosis and neuroinflammation via up-regulating menin in HT22 cells.Journal of physiology and biochemistry · 2024Article
- Scientific Landscape of Oxidative Stress in Stroke: From a Bibliometric Analysis to an in-Depth Review.Neurochemical research · 2023Review
- Focal ischemic stroke modifies microglia-derived exosomal miRNAs: potential role of mir-212-5p in neuronal protection and functional recovery.Biological research · 2023Article
- Thioredoxin-1 promotes the restoration of alveolar bone in periodontitis with diabetes.iScience · 2023Article
- The effect of thioredoxin-1 in a rat model of traumatic brain injury depending on diurnal variation.Brain and behavior · 2023Article
- RIPK1-Induced A1 Reactive Astrocytes in Brain in MPTP-Treated Murine Model of Parkinson's Disease.Brain sciences · 2023Article
- Regulated necrosis pathways: a potential target for ischemic stroke.Burns & trauma · 2023Review
- Pharmacological intervention of curcumin via the NLRP3 inflammasome in ischemic stroke.Frontiers in pharmacology · 2023Review
- Mitochondrial dysfunctions induce PANoptosis and ferroptosis in cerebral ischemia/reperfusion injury: from pathology to therapeutic potential.Frontiers in cellular neuroscience · 2023Review
- Microglial Dysfunction in Neurodegenerative Diseases via RIPK1 and ROS.Antioxidants (Basel, Switzerland) · 2022Review
- Necroptosis: A Pathogenic Negotiator in Human Diseases.International journal of molecular sciences · 2022Review
- Inflammatory Responses After Ischemic Stroke.Seminars in immunopathology · 2022Review
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Microglia are rapidly activated following ischaemic stroke and participate in the induction of neuroinflammation, which exacerbates the injury of ischaemic stroke. However, the mechanisms regulating ischaemic microglia remain unclear. In the present study, middle cerebral artery occlusion and oxygen and glucose deprivation models were established for in vivo and vitro monitoring of experimental stroke. We applied recombinant human thioredoxin-1 (rhTrx-1) and Necrostatin-1 (Nec-1, inhibitor of RIPK1) to examine the role of receptor-interacting protein kinase 1 (RIPK1) in the development of inflammation in ischaemic microglia via explored the inflammatory responses and the associated mechanisms. Molecular docking results indicated that rhTrx-1 could directly bind to RIPK1. In vivo and vitro data revealed that rhTrx-1 reduced necroptosis, mitochondrial membrane potential damage, reactive oxygen species accumulation and NLR Family, pyrin domain-containing 3 protein (NLRP3) inflammasome activation and regulated the microglial M1/M2 phenotypic changes by inhibiting RIPK1 expression in ischaemic microglia. Consistent with these findings, further in vivo experiments revealed that rhTrx-1 treatment attenuated cerebral ischaemic injury by inhibiting the inflammatory response. Our data demonstrated the role of RIPK1 in microglia-induced neuroinflammation following cerebral ischaemia. Administration of rhTrx-1 provides neuroprotection in ischaemic stroke-induced microglial neuroinflammation by inhibiting RIPK1 expression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.