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10.1016/j.celrep.2021.109020 http://scihub22266oqcxt.onion/10.1016/j.celrep.2021.109020 33852916!8020087!33852916     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Rep 2021 ; 35 (3): 109020 Nephropedia Template TP {{tp|p=33852916|t=2021. Hypoxic and pharmacological activation of HIF inhibits SARS-CoV-2 infection of lung epithelial cells |pdf=|usr=}}{{33852916}} gab.com Text Hypoxic and pharmacological activation of HIF inhibits SARS-CoV-2 infection of lung epithelial cells JO: Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=33852916 #FOAvip COVID-19, caused by the novel coronavirus SARS-CoV-2, is a global health issue with more than 2 million fatalities to date. Viral replication is shaped by the cellular microenvironment, and one important factor to consider is oxygen tension, in which hypoxia inducible factor (HIF) regulates transcriptional responses to hypoxia. SARS-CoV-2 primarily infects cells of the respiratory tract, entering via its spike glycoprotein binding to angiotensin-converting enzyme 2 (ACE2). We demonstrate that hypoxia and the HIF prolyl hydroxylase inhibitor Roxadustat reduce ACE2 expression and inhibit SARS-CoV-2 entry and replication in lung epithelial cells via an HIF-1alpha-dependent pathway. Hypoxia and Roxadustat inhibit SARS-CoV-2 RNA replication, showing that post-entry steps in the viral life cycle are oxygen sensitive. This study highlights the importance of HIF signaling in regulating multiple aspects of SARS-CoV-2 infection and raises the potential use of HIF prolyl hydroxylase inhibitors in the prevention or treatment of COVID-19. Twit Text FOAVip Hypoxic and pharmacological activation of HIF inhibits SARS-CoV-2 infection of lung epithelial cells ????Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=33852916 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33852916 #FOAvip English Wikipedia <ref>{{Cite pmid|33852916}}</ref> Hypoxic and pharmacological activation of HIF inhibits SARS-CoV-2 infection of lung epithelial cells #MMPMID33852916 Wing PAC; Keeley TP; Zhuang X; Lee JY; Prange-Barczynska M; Tsukuda S; Morgan SB; Harding AC; Argles ILA; Kurlekar S; Noerenberg M; Thompson CP; Huang KA; Balfe P; Watashi K; Castello A; Hinks TSC; James W; Ratcliffe PJ; Davis I; Hodson EJ; Bishop T; McKeating JA Cell Rep 2021[Apr]; 35 (3): 109020 PMID33852916show ga COVID-19, caused by the novel coronavirus SARS-CoV-2, is a global health issue with more than 2 million fatalities to date. Viral replication is shaped by the cellular microenvironment, and one important factor to consider is oxygen tension, in which hypoxia inducible factor (HIF) regulates transcriptional responses to hypoxia. SARS-CoV-2 primarily infects cells of the respiratory tract, entering via its spike glycoprotein binding to angiotensin-converting enzyme 2 (ACE2). We demonstrate that hypoxia and the HIF prolyl hydroxylase inhibitor Roxadustat reduce ACE2 expression and inhibit SARS-CoV-2 entry and replication in lung epithelial cells via an HIF-1alpha-dependent pathway. Hypoxia and Roxadustat inhibit SARS-CoV-2 RNA replication, showing that post-entry steps in the viral life cycle are oxygen sensitive. This study highlights the importance of HIF signaling in regulating multiple aspects of SARS-CoV-2 infection and raises the potential use of HIF prolyl hydroxylase inhibitors in the prevention or treatment of COVID-19. |A549 Cells[MESH] |Animals[MESH] |COVID-19 Drug Treatment[MESH] |COVID-19/*metabolism/pathology[MESH] |Caco-2 Cells[MESH] |Cell Hypoxia/drug effects[MESH] |Chlorocebus aethiops[MESH] |Epithelial Cells/*metabolism/virology[MESH] |Glycine/*analogs & derivatives/pharmacology[MESH] |Humans[MESH] |Hypoxia-Inducible Factor 1, alpha Subunit/*metabolism[MESH] |Isoquinolines/*pharmacology[MESH] |Lung/*metabolism/virology[MESH] |Mice[MESH] |SARS-CoV-2/*physiology[MESH] |Vero Cells[MESH] |Virus Internalization/*drug effects[MESH]Hypoxic and pharmacological activation of HIF inhibits SARS-CoV-2 infe(epmc).pdf DeepDyve Pubget Overpricing