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10.1186/s41232-020-00146-3

http://scihub22266oqcxt.onion/10.1186/s41232-020-00146-3
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33014208!7527296!33014208
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suck abstract from ncbi


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pmid33014208      Inflamm+Regen 2020 ; 40 (ä): 37
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  • How COVID-19 induces cytokine storm with high mortality #MMPMID33014208
  • Hojyo S; Uchida M; Tanaka K; Hasebe R; Tanaka Y; Murakami M; Hirano T
  • Inflamm Regen 2020[]; 40 (ä): 37 PMID33014208show ga
  • 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-kappaB) pathway and stimulated by the simultaneous activation of IL-6-signal transducer and activator of transcription 3 (STAT3) and NF-kappaB 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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