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- W2932848164 endingPage "591" @default.
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- W2932848164 abstract "Inflammation is a devastating pathophysiological process during stroke, a devastating disease that is the second most common cause of death worldwide. Activation of the NOD-like receptor protein (NLRP3)-infammasome has been proposed to mediate inflammatory responses during ischemic stroke. Briefly, NLRP3 inflammasome activates caspase-1, which cleaves both pro-IL-1 and pro-IL-18 into their active pro-inflammatory cytokines that are released into the extracellular environment. Several NLRP3 inflammasome inhibitors have been promoted, including small molecules, type I interferon, micro RNAs, nitric oxide, and nuclear factor erythroid-2 related factor 2 (Nrf2), some of which are potentially efficacious clinically. This review will describe the structure and cellular signaling pathways of the NLRP3 inflammasome during ischemic stroke, and current evidence for NLRP3 inflammasome inhibitors." @default.
- W2932848164 created "2019-04-11" @default.
- W2932848164 creator A5020367370 @default.
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- W2932848164 creator A5062326562 @default.
- W2932848164 creator A5065424164 @default.
- W2932848164 creator A5069899769 @default.
- W2932848164 date "2019-04-02" @default.
- W2932848164 modified "2023-10-06" @default.
- W2932848164 title "NLRP3 inflammasome in ischemic stroke: As possible therapeutic target" @default.
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