ArticleCell reports. Medicine2026
Identifying the role of NLRP3 inflammasome in stroke progression and outcome before recanalization.
Article in Cell reports. Medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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1 citing paper in PubMed.
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9 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Acute ischemic stroke (AIS) induces a rapid inflammatory response that partly counteracts the beneficial effects of recanalization by endovascular thrombectomy (EVT). The molecular triggers of inflammation in AIS are still elusive. We analyze the role of the NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasome before recanalization. NLRP3-mRNA levels increase rapidly in the ischemic brain following permanent middle cerebral artery occlusion in mice. NLRP3 protein is primarily expressed by intravascular neutrophils and cerebral endothelium. Blocking NLRP3 activation with the small molecule MCC950 reduces infarct progression and inflammation significantly already during large vessel occlusion. In human AIS, we find similarly increased NLRP3 expression in accumulating leukocytes within pial blood samples taken from the secluded ischemic brain territory immediately before recanalization. The number of NLRP3-positive cells before EVT predicts stroke outcome after 3 months. Our results identify NLRP3 as a promising therapeutic target to attenuate rapid infarct progression prior to recanalization.
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