ArticleScientific reports2018
Inhibition of the NLRP3-inflammasome as a potential approach for neuroprotection after stroke.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers, 1 of them a synthesis that pooled it.
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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
134 citing papers in PubMed, 1 synthesis or guideline pooled it, 233 citations in OpenAlex.
- Macrophages in Renal Injury, Repair, Fibrosis Following Acute Kidney Injury and Targeted Therapy.Frontiers in immunology · 2022Pooled it
- LncRNA HOTAIR/miR-9-5p/FOXP1 axis modulates cerebral ischemia-reperfusion injury via NLRP3 inflammasome activation.IBRO neuroscience reports · 2026Article
- Targeting Microglial HDAC5 Suppresses NLRP3 Inflammation via NF-κB Deacetylation to Alleviate Ischemic Brain Injury.CNS neuroscience & therapeutics · 2026Article
- NLRP3 Regulation in Neonatal Hypoxic-Ischemic Encephalopathy-Focus on Microglial Activation.International journal of molecular sciences · 2026Article
- NLRP3 Marks an Inflammatory Neutrophil-NETosis-Pyroptosis Network in Human Ischemic Stroke Thrombi.Cells · 2026Article
- Therapeutic Potential of NLRP3 Inhibitor MCC950 in Aging Mice Stroke Outcomes.Translational stroke research · 2026Article
- Identifying the role of NLRP3 inflammasome in stroke progression and outcome before recanalization.Cell reports. Medicine · 2026Article
- Stroke in persistent chronic kidney disease condition alters innate-immunity to escalate mitochondrial dysfunction and aging.npj aging · 2026Article
- Targeting the Biology of Aging in Cerebrovascular Disease: Inflammation, Metabolism, Senescence, and Regeneration.International journal of molecular sciences · 2026Review
- Neurogenesis and Neuroinflammation in Dialogue: Mapping Gaps, Modulating Microglia, Rewiring Aging.Cells · 2026Review
- PANoptosis in neurological disorders: from inflammatory cell death mechanisms to neuroprotective strategies.Frontiers in neuroscience · 2026Review
- Microglial immunosurveillance after ischemic stroke: dynamic phenotypes, neurovascular interactions, and therapeutic opportunities.Frontiers in immunology · 2026Review
- The Mechanism of Carboxypeptidase E Regulating NLRP3 Inflammasome Signaling in the Pathogenesis of Depression-Like Behaviors in Mice.Neuroimmunomodulation · 2026Article
- NLRP3 Inflammasome Activation in Oxidative Stress: A Key Mechanism Driving Neuroinflammation.Neuroimmunomodulation · 2026Review
- PANoptosis and mitochondrial regulatory mechanisms in cerebral ischemia-reperfusion injury.Frontiers in physiology · 2026Review
- Inflammatory Mechanisms in Acute Coronary Syndromes: From Pathophysiology to Therapeutic Targets.Cells · 2025Review
- Elevated serum NLRP3 inflammasome level potentially predicts haemorrhagic transformation and unfavourable outcome in acute ischemic stroke patients.Annals of medicine · 2025Article
- Microglial Annexin A3 Downregulation Alleviates Ischemic Injury by Inhibiting NF-κB/NLRP3-mediated Inflammation.Inflammation · 2025Article
- Chronic Ketosis Provides Neuroprotection Through HIF- 1α-Mediated Control of the TXNIP/NLRP3 Axis by Regulating the Inflammatory and Apoptotic Response.Molecular neurobiology · 2025Article
- Systemic inflammation as a central player in the initiation and development of Alzheimer's disease.Immunity & ageing : I & A · 2025Review
74 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
Abstract
Activation of the NOD-like receptor protein (NLRP3)-inflammasome has been postulated to mediate inflammatory responses to brain damage during ischemic/reperfusion (I/R) injury. We therefore hypothesized that MCC950, a selective NLRP3-inflammasome inhibitor provides protection in mouse model of transient middle cerebral artery occlusion (tMCAO). Focal cerebral ischemia was induced by 60 min tMCAO followed by intraperitoneal administration of MCC950 (50 mg/kg) or saline at 1 h and 3 h post-occlusion. After 24 h of I/R, mice were tested for neurological outcome and were sacrificed for the analysis of infarct size and estimating NLRP3-inflammasome and apoptotic markers as well. Spectrophotometric method was used to determine hemoglobin (Hb) content as a marker of intracerebral hemorrhage. MCC950-treated mice showed a substantial reduction in infarction, edema and Hb content compared to saline controls in parallel with improved neurological deficits. MCC950 reduced expression of NLRP3-inflammasome cleavage products Caspase-1 and interlukin-1β (IL-1β) in penumbral region. These protective effects of MCC950 were associated with decreased TNF-α levels as well as poly (ADP-ribose) polymerase (PARP) and Caspase-3 cleavage and paralleled less phosphrylated NFκBp65 and IκBα levels. Taken together, these data indicate that inhibition of NLRP3-inflammasome with MCC950 has therapeutic potential in ischemic stroke models. Further investigations into the therapeutic efficacy and protocols are needed to confirm whether MCC950 treatment could be a promising candidate for clinical trials.
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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.