{"title":"游离 DNA 激活二级中风机制","authors":"Ian Fyfe","doi":"10.1038/s41582-024-01020-3","DOIUrl":null,"url":null,"abstract":"<p>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.</p>","PeriodicalId":19085,"journal":{"name":"Nature Reviews Neurology","volume":null,"pages":null},"PeriodicalIF":28.2000,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Free DNA activates secondary stroke mechanism\",\"authors\":\"Ian Fyfe\",\"doi\":\"10.1038/s41582-024-01020-3\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p>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.</p>\",\"PeriodicalId\":19085,\"journal\":{\"name\":\"Nature Reviews Neurology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":28.2000,\"publicationDate\":\"2024-09-12\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Nature Reviews Neurology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1038/s41582-024-01020-3\",\"RegionNum\":1,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"CLINICAL NEUROLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Nature Reviews Neurology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1038/s41582-024-01020-3","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
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.
期刊介绍：
Nature Reviews Neurology aims to be the premier source of reviews and commentaries for the scientific and clinical communities we serve. We want to provide an unparalleled service to authors, referees, and readers, and we work hard to maximize the usefulness and impact of each article. The journal publishes Research Highlights, Comments, News & Views, Reviews, Consensus Statements, and Perspectives relevant to researchers and clinicians working in the field of neurology. Our broad scope ensures that the work we publish reaches the widest possible audience. Our articles are authoritative, accessible, and enhanced with clearly understandable figures, tables, and other display items. This page gives more detail about the aims and scope of the journal.
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