International Journal of Biological Sciences · 2025 · 17 citations · 40 references
Life SciencesCell BiologyImmunologyAutophagyInflammationInnate ImmunityInflammasome ActivationInflammatory Cell SignalingInflammatory MediatorsInflammatory SignalingMitophagySepsis PathophysiologyFundc1-mediated MitophagyInflammasome Inhibition MechanismsMacrophage Inflammasome ActivationNlr Family Pyrin Domain-containing 3 InflammasomeNlrp3 InflammasomePro-inflammatory Signaling PathwaysSepsis PathologySepsis-associated Inflammation
, emodin confers significant protection in sepsis models, with these protective effects being lost in NLRP3-deficient mice or upon macrophage-specific deletion of FUNDC1. Collectively, our findings uncover a novel CK2-FUNDC1-mitophagy axis through which emodin inhibits NLRP3 inflammasome activation, highlighting its promise as a clinically translatable candidate for the treatment of NLRP3-driven inflammatory diseases.
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