How COVID-19 induces cytokine storm with high mortality.

How COVID-19 induces cytokine storm with high mortality.
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DOI:
10.1186/s41232-020-00146-3
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发表时间:
2020
影响因子:
8.1
通讯作者:
Hirano T
Hirano T
中科院分区:
医学3区
文献类型:
--
作者:
Hojyo S;Uchida M;Tanaka K;Hasebe R;Tanaka Y;Murakami M;Hirano T

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由严重急性呼吸综合征冠状病毒2型(SARS-CoV-2)引起的新型冠状病毒病2019(COVID-19)首次在中国武汉报道,但已迅速蔓延至全球。一些COVID-19患者会出现严重的急性呼吸窘迫综合征(ARDS)症状,死亡率很高。这种高严重程度依赖于细胞因子风暴,最可能由白细胞介素-6(IL-6)放大器诱导,这是一种调节核因子κ B(NF-κB)通路的超活化机制,并受到非免疫细胞(包括肺泡上皮细胞和内皮细胞)中IL-6信号转导和转录激活因子3(STAT 3)和NF-κB信号传导的同时活化的刺激。我们假设IL-6-STAT 3信号传导是COVID-19中细胞因子风暴的有希望的治疗靶点,因为IL-6是主要的STAT 3刺激物,特别是在炎症期间。本文就COVID-19患者ARDS的发病机制和潜在治疗靶点进行综述。
The newly emerging coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was first reported in Wuhan, China, but has rapidly spread all over the world. Some COVID-19 patients encounter a severe symptom of acute respiratory distress syndrome (ARDS) with high mortality. This high severity is dependent on a cytokine storm, most likely induced by the interleukin-6 (IL-6) amplifier, which is hyper-activation machinery that regulates the nuclear factor kappa B (NF-κB) pathway and stimulated by the simultaneous activation of IL-6-signal transducer and activator of transcription 3 (STAT3) and NF-κB signaling in non-immune cells including alveolar epithelial cells and endothelial cells. We hypothesize that IL-6-STAT3 signaling is a promising therapeutic target for the cytokine storm in COVID-19, because IL-6 is a major STAT3 stimulator, particularly during inflammation. We herein review the pathogenic mechanism and potential therapeutic targets of ARDS in COVID-19 patients.
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