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IRF3 and type I interferons fuel a fatal response to myocardial infarction
Nature Medicine ( IF 58.7 ) Pub Date : 2017-11-06 , DOI: 10.1038/nm.4428
Kevin R King , Aaron D Aguirre , Yu-Xiang Ye , Yuan Sun , Jason D Roh , Richard P Ng , Rainer H Kohler , Sean P Arlauckas , Yoshiko Iwamoto , Andrej Savol , Ruslan I Sadreyev , Mark Kelly , Timothy P Fitzgibbons , Katherine A Fitzgerald , Timothy Mitchison , Peter Libby , Matthias Nahrendorf , Ralph Weissleder

IRF3 and type I interferons fuel a fatal response to myocardial infarction

IRF3 and type I interferons fuel a fatal response to myocardial infarction, Published online: 06 November 2017; doi:10.1038/nm.4428

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The massive cell death that occurs during myocardial infarction releases self-DNA and triggers an interferon response in infiltrating leukocytes via a cGAS–STING–IRF3 pathway. Interference with this response—either by genetic disruption of the pathway or antibody blockade of the type I interferon receptor—is beneficial in mice subjected to myocardial infarction.

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中文翻译:

IRF3和I型干扰素助长了对心肌梗死的致命反应

IRF3和I型干扰素助长了对心肌梗死的致命反应

IRF3和I型干扰素助长了对心肌梗死的致命反应,在线发布:2017年11月6日;doi:10.1038 / nm.4428

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心肌梗死期间发生的大量细胞死亡释放出自身DNA,并通过cGAS–STING–IRF3途径触发了浸润性白细胞的干扰素反应。通过遗传途径的干扰或I型干扰素受体的抗体阻断来干扰这种反应,在遭受心肌梗塞的小鼠中是有益的。

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更新日期:2017-11-06
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