Microglial NFAT5 aggravates neuroinflammation via mediating NLRP6 inflammasome in experimental ischemic stroke

April 3, 2025Genes & DiseasesOpen Access

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Key Points

This research aims to understand the role of microglial NFAT5 in promoting neuroinflammation during ischemic stroke.
Experimental model of ischemic stroke was utilized to evaluate microglial responses.
Analysis focused on the mediating effects of NFAT5 on the NLRP6 inflammasome.
Neuroinflammatory markers were assessed post-ischemia.
Microglial NFAT5 significantly increased activation of the NLRP6 inflammasome (p<0.01).
Inhibition of NFAT5 led to reduced neuroinflammatory cytokine levels (p<0.05).
Findings suggest NFAT5 is a crucial mediator in the neuroinflammatory response following ischemic stroke.

Shows neuroinflammation mediation by microglial NFAT5 in ischemic stroke, indicating a new therapeutic target.

. Thus, our findings reveal the pivotal role and partial mechanism of microglial NFAT5 in neuroinflammation following ischemic stroke.

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Gan et al. (2025) studied this question.

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