血小板与中性粒细胞胞外陷阱之间的反馈回路会加剧严重脓毒症中的炎症反应。
A feedback loop between platelets and NETs amplifies inflammation in severe sepsis.
出版信息
Nat Cardiovasc Res. 2022;1(8):698-699. doi: 10.1038/s44161-022-00110-z. Epub 2022 Aug 8.
Abstract
Sepsis-derived S100A8/A9 induces GSDMD-dependent platelet pyroptosis via the TLR4-ROS-NLRP3-caspase 1 pathway, leading to the release of oxidized mitochondrial DNA that contributes to the formation of neutrophil extracellular traps (NETs). NETs in turn release S100A8/A9 and accelerate platelet pyroptosis, forming a positive feedback loop and thereby amplifying the production of proinflammatory cytokines.
摘要
脓毒症衍生的S100A8/A9通过TLR4-ROS-NLRP3-半胱天冬酶1途径诱导依赖Gasdermin D的血小板焦亡，导致氧化线粒体DNA释放，这有助于中性粒细胞胞外诱捕网（NETs）的形成。NETs继而释放S100A8/A9并加速血小板焦亡，形成正反馈回路，从而放大促炎细胞因子的产生。
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