ArticleStroke2019
Extent of Ischemic Brain Injury After Thrombotic Stroke Is Independent of the NLRP3 (NACHT, LRR and PYD Domains-Containing Protein 3) Inflammasome.
Article in Stroke, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 52 citations in OpenAlex.
- Interleukin-1 regulates myeloid cell trafficking and cerebral blood flow following intracerebral haemorrhage.Disease models & mechanisms · 2025Article
- Low-Frequency (1 Hz) Repetitive Trans-Spinal Magnetic Stimulation Attenuates NLRP3-Driven Neuroinflammation and Enhances Motor Recovery in Spinal Cord-Injured Mice.Journal of inflammation research · 2025Article
- From disruption to remodeling: the evolution and therapeutic prospects of Neuroimmune Regulatory Circuitry after ischemic stroke.Frontiers in immunology · 2025Review
- Biological and therapeutic significance of targeting NLRP3 inflammasome in the brain and the current efforts to develop brain-penetrant inhibitors.Advances in pharmacology (San Diego, Calif.) · 2025Review
- Activation of Inflammasomes and Relevant Modulators for the Treatment of Microglia-mediated Neuroinflammation in Ischemic Stroke.Molecular neurobiology · 2024Review
- Cortical microinfarcts potentiate recurrent ischemic injury through NLRP3-dependent trained immunity.Cell death & disease · 2024Article
- Article
- Review
- Argon mitigates post-stroke neuroinflammation by regulating M1/M2 polarization and inhibiting NF-κB/NLRP3 inflammasome signaling.Journal of molecular cell biology · 2023Article
- 12/15-lipoxygenase inhibition attenuates neuroinflammation by suppressing inflammasomes.Frontiers in cellular neuroscience · 2023Article
- The role of NLRP3 inflammasome-mediated pyroptosis in ischemic stroke and the intervention of traditional Chinese medicine.Frontiers in pharmacology · 2023Review
- Itaconate and fumarate derivatives inhibit priming and activation of the canonical NLRP3 inflammasome in macrophages.Immunology · 2022Article
- Electroacupuncture Inhibits NLRP3 Activation by Regulating CMPK2 After Spinal Cord Injury.Frontiers in immunology · 2022Article
- Role of inflammasomes in neuroinflammation after ischemic stroke.Encephalitis (Seoul, Korea) · 2021Review
- Role of microglial and endothelial CD36 in post-ischemic inflammasome activation and interleukin-1β-induced endothelial activation.Brain, behavior, and immunity · 2021Article
- Intra-arterial Stem Cell Therapy Diminishes Inflammasome Activation After Ischemic Stroke: a Possible Role of Acid Sensing Ion Channel 1a.Journal of molecular neuroscience : MN · 2021Article
- Temporal and Spatial Dynamics of Inflammasome Activation After Ischemic Stroke.Frontiers in neurology · 2021Article
- Janus Kinase Inhibition Ameliorates Ischemic Stroke Injury and Neuroinflammation Through Reducing NLRP3 Inflammasome ActivationFrontiers in immunology · 2021Article
- NLRP3-dependent microglial training impaired the clearance of amyloid-beta and aggravated the cognitive decline in Alzheimer's disease.Cell death & disease · 2020Article
- Neuroinflammation and fibrosis in stroke: The good, the bad and the ugly.Journal of neuroimmunology · 2020Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Background and Purpose- A major process contributing to cell death in the ischemic brain is inflammation. Inflammasomes are multimolecular protein complexes that drive inflammation through activation of proinflammatory cytokines, such as IL (interleukin)-1β. Preclinical evidence suggests that IL-1β contributes to a worsening of ischemic brain injury. Methods- Using a mouse middle cerebral artery thrombosis model, we examined the inflammatory response after stroke and the contribution of the NLRP3 (NACHT, LRR and PYD domains-containing protein 3) inflammasome to ischemic injury. Results- There was a marked inflammatory response after stroke characterized by increased expression of proinflammatory cytokines and NLRP3 and by recruitment of leukocytes to the injured tissue. Targeting NLRP3 with the inhibitor MCC950, or using mice in which NLRP3 was knocked out, had no effect on the extent of injury caused by stroke. Conclusions- These data suggest that the NLRP3 pathway does not contribute to the inflammation exacerbating ischemic brain damage, contradicting several recent reports to the contrary.
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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.