After a stroke, circulating, cell-free DNA causes inflammasome activation in atherosclerotic plaques that can lead to recurrent stroke, work in a mouse model has shown. In a model of stroke-induced recurrent ischaemia, increased inflammation in plaques in the common carotid artery resulted from activation of the AIM2 inflammasome by cell-free DNA that primarily originated from neutrophil extracellular traps (NETs). The increased inflammation led to plaque rupture and a secondary stroke. Administration of DNase after stroke reduced the risk of recurrent events in the mice, suggesting that this mechanism could be targeted therapeutically.

中文翻译：

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游离 DNA 激活次级卒中机制

小鼠模型中的工作表明，中风后循环的游离 DNA 会导致动脉粥样硬化斑块中的炎性小体激活，从而导致复发性中风。在中风诱导的复发性缺血模型中，颈总动脉斑块炎症增加是由于主要源自中性粒细胞胞外陷阱 （NET） 的游离 DNA 激活 AIM2 炎性小体。炎症增加导致斑块破裂和继发性中风。中风后施用 DNase 降低了小鼠复发事件的风险，表明这种机制可以针对治疗。