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- W4310366950 abstract "Stroke is a leading cause of death worldwide that can result from arterial and cardiac causes. The inflammatory response is a significant contributor to the damage found in the ischemic penumbra that forms after stroke. The inflammasome plays an important role in mounting an innate immune response after cerebral ischemia, and inflammasome inhibition has been associated with improved outcomes (decreased infarct volume, decreased inflammation, and improved functional recovery) in animal models of stroke. Here we describe the pathophysiology of stroke, how different inflammasomes such as the NLRP1, NLPR3, AIM2, and NLRC4 inflammasomes are involved in mediating the inflammatory response through the activation of interleukin (IL)-1β and IL-18 as well as the inflammasome-mediated cell death process of pyroptosis, and we present findings from human studies in the context of stroke. Moreover, we present potential therapeutics that have been associated with improved stroke outcomes by inhibiting inflammasome signaling." @default.
- W4310366950 created "2022-12-09" @default.
- W4310366950 creator A5004112847 @default.
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- W4310366950 date "2023-01-01" @default.
- W4310366950 modified "2023-09-26" @default.
- W4310366950 title "The inflammasome in stroke" @default.
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- W4310366950 doi "https://doi.org/10.1016/b978-0-323-91802-2.00030-x" @default.
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