ArticleCell death discovery2026
Nrf2 promotes NLRP3 inflammasome assembly and activation by Klf9-TXNIP axis.
Article in Cell death discovery, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
NLRP3 inflammasome activation shows a crucial role in the innate immune response that triggers inflammation. Activation is controlled by two sequential steps: a priming step, followed by an assembly step. Nrf2 has been shown to promote NLRP3 inflammasome activation; however, the underlying mechanisms remain elusive. This study identifies Nrf2 as an encourager of NLRP3 inflammasome activation. We show that Nrf2 inhibition suppresses NLRP3 inflammasome activation in macrophages, including THP-1 cells and BMDMs. In addition, Nrf2 facilitates NLRP3 inflammasome assembly. Mechanically, Nrf2 increases Klf9 expression by binding to the Klf9 promoter. Klf9 stabilizes TXNIP by deubiquitination, thereby enhancing the TXNIP-NLRP3 interaction, which is required for NLRP3 inflammasome assembly and full activation. Finally, Nrf2 deficiency exerts a protective effect and alleviates NLRP3 inflammasome activation in mouse models of DSS-induced colitis and MSU crystals-induced acute gouty arthritis. Our study reveals a novel regulatory mechanism of NLRP3 inflammasome by Nrf2 and indicates Nrf2 may be a promising target for treating NLRP3 inflammasome-driven diseases.
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