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10.1172/jci.insight.155896 http://scihub22266oqcxt.onion/10.1172/jci.insight.155896 35076028!8855831!35076028     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       JCI+Insight 2022 ; 7 (2): ä Nephropedia Template TP {{tp|p=35076028|t=2022. Impairing RAGE signaling promotes survival and limits disease pathogenesis following SARS-CoV-2 infection in mice |pdf=|usr=}}{{35076028}} gab.com Text Impairing RAGE signaling promotes survival and limits disease pathogenesis following SARS-CoV-2 infection in mice JO: JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=35076028 #FOAvip Cellular and molecular mechanisms driving morbidity following SARS-CoV-2 infection have not been well defined. The receptor for advanced glycation end products (RAGE) is a central mediator of tissue injury and contributes to SARS-CoV-2 disease pathogenesis. In this study, we temporally delineated key cell and molecular events leading to lung injury in mice following SARS-CoV-2 infection and assessed efficacy of therapeutically targeting RAGE to improve survival. Early following infection, SARS-CoV-2 replicated to high titers within the lungs and evaded triggering inflammation and cell death. However, a significant necrotic cell death event in CD45- populations, corresponding with peak viral loads, was observed on day 2 after infection. Metabolic reprogramming and inflammation were initiated following this cell death event and corresponded with increased lung interstitial pneumonia, perivascular inflammation, and endothelial hyperplasia together with decreased oxygen saturation. Therapeutic treatment with the RAGE antagonist FPS-ZM1 improved survival in infected mice and limited inflammation and associated perivascular pathology. Together, these results provide critical characterization of disease pathogenesis in the mouse model and implicate a role for RAGE signaling as a therapeutic target to improve outcomes following SARS-CoV-2 infection. Twit Text FOAVip Impairing RAGE signaling promotes survival and limits disease pathogenesis following SARS-CoV-2 infection in mice ????JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=35076028 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=35076028 #FOAvip English Wikipedia <ref>{{Cite pmid|35076028}}</ref> Impairing RAGE signaling promotes survival and limits disease pathogenesis following SARS-CoV-2 infection in mice #MMPMID35076028 Jessop F; Schwarz B; Scott D; Roberts LM; Bohrnsen E; Hoidal JR; Bosio CM JCI Insight 2022[Jan]; 7 (2): ä PMID35076028show ga Cellular and molecular mechanisms driving morbidity following SARS-CoV-2 infection have not been well defined. The receptor for advanced glycation end products (RAGE) is a central mediator of tissue injury and contributes to SARS-CoV-2 disease pathogenesis. In this study, we temporally delineated key cell and molecular events leading to lung injury in mice following SARS-CoV-2 infection and assessed efficacy of therapeutically targeting RAGE to improve survival. Early following infection, SARS-CoV-2 replicated to high titers within the lungs and evaded triggering inflammation and cell death. However, a significant necrotic cell death event in CD45- populations, corresponding with peak viral loads, was observed on day 2 after infection. Metabolic reprogramming and inflammation were initiated following this cell death event and corresponded with increased lung interstitial pneumonia, perivascular inflammation, and endothelial hyperplasia together with decreased oxygen saturation. Therapeutic treatment with the RAGE antagonist FPS-ZM1 improved survival in infected mice and limited inflammation and associated perivascular pathology. Together, these results provide critical characterization of disease pathogenesis in the mouse model and implicate a role for RAGE signaling as a therapeutic target to improve outcomes following SARS-CoV-2 infection. |*COVID-19 Drug Treatment[MESH] |*COVID-19/genetics/metabolism[MESH] |*Lung/metabolism/virology[MESH] |*Receptor for Advanced Glycation End Products/antagonists & inhibitors/genetics/metabolism[MESH] |Animals[MESH] |Benzamides/*pharmacology[MESH] |Disease Models, Animal[MESH] |Mice[MESH] |Mice, Transgenic[MESH] |SARS-CoV-2/*physiology[MESH] |Signal Transduction/*drug effects[MESH]Impairing RAGE signaling promotes survival and limits disease pathogen(epmc).pdf DeepDyve Pubget Overpricing