ReviewInflammation research : official journal of the European Histamine Research Society ... [et al.]2025
The role of NLRP3 inflammasome-mediated pyroptosis in astrocytes during hyperoxia-induced brain injury.
Review in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Dissecting PANoptosis in the Nervous System: A Unified Cell-Death Mechanism Driving Neuroimmune Activation and Chronic Neuroinflammation.Molecular neurobiology · 2026Review
- Pyroptosis in endometritis: Molecular mechanisms, pathogenic roles, and therapeutic opportunities.iScience · 2026Review
- The aging gut-glia-immune axis in alzheimer's disease: microbiome-derived mediators of neuroinflammation and therapeutic innovation.GeroScience · 2026Review
- Astrocyte-mediated inflammatory responses in traumatic brain injury: mechanisms and potential interventions.Frontiers in immunology · 2025Review
- Viral reprogramming of glial metabolism as a driver of neuroinflammation.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
backgroundHyperoxia-induced brain injury is a severe neurological complication that is often accompanied by adverse long-term prognosis. The pathogenesis of hyperoxia-induced brain injury is highly complex, with neuroinflammation playing a crucial role. The activation of the nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome, which plays a pivotal role in regulating and amplifying the inflammatory response, is the pathological core of hyperoxia-induced brain injury. Additionally, astrocytes actively participate in neuroinflammatory responses. However, there is currently no comprehensive overview summarizing the role of astrocytes in hyperoxia-induced brain injury and the NLRP3 signaling pathways in astrocytes.
objectiveThis article aims to provide an overview of studies reported in the literature investigating the pathological role of astrocyte involvement during the inflammatory response in hyperoxia-induced brain injury, the mechanisms of hyperoxia activateing the NLRP3 inflammasome to mediate pyroptosis in astrocytes, and the potential therapeutic effects of drugs targeting the NLRP3 inflammasome to alleviate hyperoxia-induced brain injury.
methodWe searched major databases (including PubMed, Web of Science, and Google Scholar, etc.) for literature encompassing astrocytes, NLRP3 inflammasome, and pyroptosis during hyperoxia-induced brain injury up to Oct 2024. We combined with studies found in the reference lists of the included studies.
conclusionIn this study, we elucidated the transition of function in astrocytes and activation mechanisms under hyperoxic conditions, and we summarized the potential upstream of the trigger involved in NLRP3 inflammasome activation during hyperoxia-induced brain injury, such as ROS and potassium efflux. Furthermore, we described the signaling pathways of the NLRP3 inflammasome and pyroptosis executed by GSDMD and GSDME in astrocytes under hyperoxic conditions. Finally, we summarized the inhibitors targeting the NLRP3 inflammasome in astrocytes to provide new insights for treating hyperoxia-induced brain injury.
Indexed as
Identifiers
39862240What Socratic holds
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 Socratic graph.