ArticleBMC neuroscience2022
NLRP3 inflammasome regulates astrocyte transformation in brain injury induced by chronic intermittent hypoxia.
Article in BMC neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Cerebral oxidative stress, inflammation and apoptosis induced by intermittent hypoxia: a systematic review and meta-analysis of rodent data.European respiratory review : an official journal of the European Respiratory Society · 2024Pooled it
- Molecular Drivers of Cognitive Decline and Neuroprotection in Obstructive Sleep Apnea: A Narrative Review.Antioxidants (Basel, Switzerland) · 2026Review
- A2 astrocyte polarization mediates ketogenic diet protection of blood-central nervous system barriers in experimental autoimmune encephalomyelitis.Neural regeneration research · 2026Article
- Sleep Disorders in Neurodegenerative Diseases: Pathological Correlations and Underlying Mechanisms.Neuroscience bulletin · 2026Review
- The roles of microglia and astrocytes in inflammasomes and neurological disorders.Neural regeneration research · 2026Article
- Inflammasome adaptor ASC promotes sustained neuroinflammation and mild cognitive impairment in a closed-head injury model.The Journal of clinical investigation · 2026Article
- Brain nitric oxide and inflammation in chronic intermittent hypoxia: Contributors to cognitive impairment and hypertension.Brain, behavior, & immunity - health · 2025Review
- Effects of Obstructive Sleep Apnea on Cognition: An Analysis of Electroencephalography Microstates and Alpha Peak Frequency.CNS neuroscience & therapeutics · 2025Article
- Ethanol consumption aggravates amyloid pathology and neuroinflammation in Alzheimer's disease associated with inflammasome activation and ASC speck propagation.Journal of neuroinflammation · 2025Article
- Association between endogenous lactate accumulation and dysregulated activation of the NLRP3 inflammasome pathway in schizophrenia.Scientific reports · 2025Observational
- Chronic Intermittent Hypoxia-Induced Neural Injury: Pathophysiology, Neurodegenerative Implications, and Therapeutic Insights.CNS neuroscience & therapeutics · 2025Review
- Association Between Fractional Exhaled Nitric Oxide (FeNO) and Cognitive Function in Patients with Obstructive Sleep Apnea.Nature and science of sleep · 2025Article
- NLRP3 Inflammasome Triggers Inflammation of Obstructive Sleep Apnea.Current molecular medicine · 2025Review
- Mechanisms of Acetate in Alleviating SETDB1-Linked Neuroinflammation and Cognitive Impairment in a Mouse Model of OSA.Journal of inflammation research · 2025Article
- Review
- Obstructive Sleep Apnea-Associated Intermittent Hypoxia-Induced Immune Responses in Males, Pregnancies, and Offspring.International journal of molecular sciences · 2024Review
- Effect of NLRP3 inflammasome induced astrocyte phenotype alteration in morphine tolerance.Frontiers in pharmacology · 2024Article
- Obstructive sleep apnea, the NLRP3 inflammasome and the potential effects of incretin therapies.Frontiers in sleep · 2024Review
- Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer's disease.Molecular neurodegeneration · 2023Review
- Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundObstructive sleep apnea (OSA) is mainly characterized by sleep fragmentation and chronic intermittent hypoxia (CIH), the latter one being associated with multiple organ injury. Recently, OSA-induced cognition dysfunction has received extensive attention from scholars. Astrocytes are essential in neurocognitive deficits via A1/A2 phenotypic changes. Nucleotide oligomerization domain (NOD)-like receptor protein 3 (NLRP3) inflammasome is considered the most important factor inducing and maintaining neuroinflammation. However, whether the NLRP3 regulates the A1/A2 transformation of astrocytes in CIH-related brain injury remains unclear.
methodsWe constructed an OSA-related CIH animal model and assessed the rats' learning ability in the Morris water maze; the histopathological assessment was performed by HE and Nissl staining. The expression of GFAP (astrocyte marker), C3d (A1-type astrocyte marker), and S100a10 (A2-type astrocyte marker) were detected by immunohistochemistry and immunofluorescence. Western blotting and RT-qPCR were used to evaluate the changes of A1/A2 astrocyte-related protein and NLRP3/Caspase-1/ASC/IL-1β.
resultsThe learning ability of rats decreased under CIH. Further pathological examination revealed that the neurocyte in the hippocampus were damaged. The cell nuclei were fragmented and dissolved, and Nissl bodies were reduced. Immunohistochemistry showed that astrocytes were activated, and morphology and number of astrocytes changed. Immunofluorescence, Western blotting and RT-qPCR showed that the expression of C3d was increased while S100a10 was decreased. Also, the expression of the inflammasome (NLRP3/Caspase-1/ASC/IL-1β) was increased. After treatment of MCC950 (a small molecule inhibitor of NLRP3), the damage of nerve cells was alleviated, the Nissl bodies increased, the activation of astrocytes was reduced, and the expression of A2-type astrocytes was increased. In contrast, A1-type astrocytes decreased, and the expression of inflammasome NLRP3/Caspase-1/ASC/IL-1β pathway-related proteins decreased.
conclusionThe NLRP3 inflammasome could regulate the A1/A2 transformation of astrocytes in brain injury induced by CIH.
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