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Fig. 2 | Journal of Neuroinflammation

Fig. 2

From: NLRP3 inflammasome as a potential treatment in ischemic stroke concomitant with diabetes

Fig. 2

Schematic overview of NLRP3 inflammasome activation mechanisms in ischemic stroke concomitant with diabetes. NLRP3 inflammasome has a crucial role in diabetes and ischemic stroke based on three canonical hypotheses—reactive oxygen species (ROS), lysosomal rupture, and cellular potassium efflux. These mechanisms may collectively activate caspase 1, which mediates the release of cytokines such as IL-1β and IL-18. Increased ROS are sensed by a complex of thioredoxin (TRX) and TRX-interacting protein (TXNIP) that can induce the dissociation of the complex. TXNIP binds to the LRR region of NLRP3, leading to NLRP3 inflammasome activation and the secretion of mature IL-1β and IL-18. The NLRP3 inflammasome is a platform for IL-1β and IL-18 production. After activation of the NLRP3 inflammasome, cells secrete a great many proinflammatory cytokines, which aggravates insulin resistance (in diabetes) and neuronal death (ischemic stroke)

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