ArticleRedox report : communications in free radical research2026
Bilirubin reduces mortality in sepsis models by inhibiting NOX2-mediated formation of neutrophil extracellular traps.
Article in Redox report : communications in free radical research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
7 authors.
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No grant is acknowledged in the PubMed record.
Abstract
objectivesSepsis is a life-threatening condition driven by a dysregulated immune response to infection, yet therapeutic options beyond antibiotics and vasopressors remain limited. Neutrophil extracellular traps (NETs) contribute significantly to sepsis-induced tissue injury, and NETosis inhibition has emerged as a potential therapeutic strategy. We hypothesized that the endogenous metabolite bilirubin mitigates inflammation in sepsis by inhibiting NETosis through targeting NOX2.
methodsTwo murine sepsis models were used to assess the effects of bilirubin on survival and systemic NETosis. Plasma NET biomarkers were quantified, and primary human neutrophils were used to validate the NETosis-inhibitory activity of bilirubin
resultsBilirubin improved survival and reduced NET biomarkers in both models. It inhibited NETosis in human neutrophils by suppressing ROS-dependent NETosis and promoting the internalization and degradation of NOX2 via endocytosis and autophagy. DISCUSSION: These findings identify bilirubin as an endogenous inhibitor of NETosis. By targeting NOX2 and suppressing NETosis, bilirubin may represent a promising therapeutic candidate for sepsis management.
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