ArticleInternational journal of biological sciences2026
Neutrophil extracellular traps prime the ZBP1-cGAS sensor complex, triggering necroptosis and inflammatory injury in acute pancreatitis.
Article in International journal of biological sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Flipons, Noncoding Transcripts and Retroelements: A Universal Host Defense.International journal of molecular sciences · 2026Review
- Review
- Bidirectional Crosstalk Between cGAS-STING and Necroptosis: From Mitochondrial DNA Release to Inflammatory Disease.Drug design, development and therapy · 2026Review
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Authors and funding
9 authors.
Funding
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Abstract
Severe acute pancreatitis (SAP) involves dynamic interactions between immune dysregulation and inflammatory infiltration. Although elevated levels of neutrophil extracellular traps (NETs) are associated with SAP, the downstream mechanisms by which NETs exacerbate the inflammatory injury remain unclear. In this study, we demonstrate that NETs levels positively correlate with SAP severity, and pharmacological inhibition of NETs reduces pancreatic injury, and acinar cell death. Mechanistically, NETs activate the ZBP1-cGAS complex via mitochondrial DNA (mtDNA), triggering downstream necroptosis and inflammatory pathways, thereby driving pancreatic inflammatory injury. Specifically, NETs induce mitochondrial damage in acinar cells, leading to cytosolic accumulation of mtDNA. This recruits ZBP1 to form a complex with cGAS dependent on the RHIM domain, wherein ZBP1 stabilizes Z-form mtDNA and potentiates cGAS recognition of Z-mtDNA, thereby cooperatively promoting necroptosis and inflammation. Furthermore, cyclosporine A inhibits mtDNA release, thereby suppressing NETs-induced ZBP1-cGAS complex formation and mitigating pancreatic injury. Our findings establish the mtDNA-ZBP1-cGAS axis as a pivotal mechanism by which NETs exacerbate pancreatic inflammation, revealing new therapeutic targets for SAP.
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