
| 10.1038/s41422-020-00435-z
http://scihub22266oqcxt.onion/10.1038/s41422-020-00435-z
 33159154!7646495!33159154
free
free
free
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Cell+Res 2020 ; 30 (12): 1078-1087 Nephropedia Template TP
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Mucus production stimulated by IFN-AhR signaling triggers hypoxia of COVID-19 #MMPMID33159154Liu Y; Lv J; Liu J; Li M; Xie J; Lv Q; Deng W; Zhou N; Zhou Y; Song J; Wang P; Qin C; Tong WM; Huang BCell Res 2020[Dec]; 30 (12): 1078-1087 PMID33159154show ga
Silent hypoxia has emerged as a unique feature of coronavirus disease 2019 (COVID-19). In this study, we show that mucins are accumulated in the bronchoalveolar lavage fluid (BALF) of COVID-19 patients and are upregulated in the lungs of severe respiratory syndrome coronavirus 2 (SARS-CoV-2)-infected mice and macaques. We find that induction of either interferon (IFN)-beta or IFN-gamma upon SARS-CoV-2 infection results in activation of aryl hydrocarbon receptor (AhR) signaling through an IDO-Kyn-dependent pathway, leading to transcriptional upregulation of the expression of mucins, both the secreted and membrane-bound, in alveolar epithelial cells. Consequently, accumulated alveolar mucus affects the blood-gas barrier, thus inducing hypoxia and diminishing lung capacity, which can be reversed by blocking AhR activity. These findings potentially explain the silent hypoxia formation in COVID-19 patients, and suggest a possible intervention strategy by targeting the AhR pathway.|Animals[MESH]|COVID-19/pathology/virology[MESH]|Cell Line[MESH]|Epithelial Cells/cytology/metabolism/virology[MESH]|Humans[MESH]|Hypoxia[MESH]|Interferon-beta/pharmacology[MESH]|Interferon-gamma/pharmacology[MESH]|Interferons/*metabolism[MESH]|Lung/metabolism/pathology[MESH]|Macaca[MESH]|Mice[MESH]|Mice, Inbred ICR[MESH]|Mice, Transgenic[MESH]|Mucins/metabolism[MESH]|Mucus/*metabolism[MESH]|Receptors, Aryl Hydrocarbon/*metabolism[MESH]|SARS-CoV-2/isolation & purification/pathogenicity[MESH]|Signal Transduction[MESH]
  
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