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10.1016/j.mehy.2020.109906 http://scihub22266oqcxt.onion/10.1016/j.mehy.2020.109906 32505910!7834360!32505910     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Med+Hypotheses 2020 ; 143 (ä): 109906 Nephropedia Template TP {{tp|p=32505910|t=2020. Novel therapeutic targets for SARS-CoV-2-induced acute lung injury: Targeting a potential IL-1beta/neutrophil extracellular traps feedback loop |pdf=|usr=}}{{32505910}} gab.com Text Novel therapeutic targets for SARS-CoV-2-induced acute lung injury: Targeting a potential IL-1beta/neutrophil extracellular traps feedback loop JO: Med Hypotheses http://www.kidney.de/pget.php?&tw=1&pmid=32505910 #FOAvip Most COVID-19 infected individuals present with mild flu-like symptoms; however, 5-10% of cases suffer from life-threatening pneumonia and respiratory failure. The pathogenesis of SARS-CoV-2 and its pathology of associated acute lung injury (ALI), acute respiratory distress syndrome (ARDS), sepsis, coagulopathy and multiorgan failure is not known. SARS-CoV-2 is an envelope virus with S (spike), M (membrane), N (nucleocapsid) and E (envelop) proteins. In a closely related coronavirus (SARS-CoV), the transmembrane E protein exerts an important role in membrane-ionic transport through viroporins, deletion of which reduced levels of IL-1beta and a remarkably reduced lung edema compared to wild type. IL-1beta is generated by macrophages upon activation of intracellular NLRP3 (NOD-like, leucine rich repeat domains, and pyrin domain-containing protein 3), part of the functional NLRP3 inflammasome complex that detects pathogenic microorganisms and stressors, while neutrophils are enhanced by increasing levels of IL-1beta. Expiring neutrophils undergo "NETosis", producing thread-like extracellular structures termed neutrophil extracellular traps (NETs), which protect against mild infections and microbes. However, uncontrolled NET production can cause acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), coagulopathy, multiple organ failure, and autoimmune disease. Herein, we present arguments underlying our hypothesis that IL-1beta and NETs, mediated via NLRP3 inflammasomes, form a feed-forward loop leading to the excessive alveolar and endothelial damage observed in severe cases of COVID-19. Considering such assertions, we propose potential drug candidates that could be used to alleviate such pathologies. Considering that recent efforts to ascertain effective treatments of COVID-19 in severe patients has been less than successful, investigating novel avenues of treating this virus are essential. Twit Text FOAVip Novel therapeutic targets for SARS-CoV-2-induced acute lung injury: Targeting a potential IL-1beta/neutrophil extracellular traps feedback loop ????Med Hypotheses http://www.kidney.de/pget.php?&tw=1&pmid=32505910 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32505910 #FOAvip English Wikipedia <ref>{{Cite pmid|32505910}}</ref> Novel therapeutic targets for SARS-CoV-2-induced acute lung injury: Targeting a potential IL-1beta/neutrophil extracellular traps feedback loop #MMPMID32505910 Yaqinuddin A; Kashir J Med Hypotheses 2020[Oct]; 143 (ä): 109906 PMID32505910show ga Most COVID-19 infected individuals present with mild flu-like symptoms; however, 5-10% of cases suffer from life-threatening pneumonia and respiratory failure. The pathogenesis of SARS-CoV-2 and its pathology of associated acute lung injury (ALI), acute respiratory distress syndrome (ARDS), sepsis, coagulopathy and multiorgan failure is not known. SARS-CoV-2 is an envelope virus with S (spike), M (membrane), N (nucleocapsid) and E (envelop) proteins. In a closely related coronavirus (SARS-CoV), the transmembrane E protein exerts an important role in membrane-ionic transport through viroporins, deletion of which reduced levels of IL-1beta and a remarkably reduced lung edema compared to wild type. IL-1beta is generated by macrophages upon activation of intracellular NLRP3 (NOD-like, leucine rich repeat domains, and pyrin domain-containing protein 3), part of the functional NLRP3 inflammasome complex that detects pathogenic microorganisms and stressors, while neutrophils are enhanced by increasing levels of IL-1beta. Expiring neutrophils undergo "NETosis", producing thread-like extracellular structures termed neutrophil extracellular traps (NETs), which protect against mild infections and microbes. However, uncontrolled NET production can cause acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), coagulopathy, multiple organ failure, and autoimmune disease. Herein, we present arguments underlying our hypothesis that IL-1beta and NETs, mediated via NLRP3 inflammasomes, form a feed-forward loop leading to the excessive alveolar and endothelial damage observed in severe cases of COVID-19. Considering such assertions, we propose potential drug candidates that could be used to alleviate such pathologies. Considering that recent efforts to ascertain effective treatments of COVID-19 in severe patients has been less than successful, investigating novel avenues of treating this virus are essential. |*Betacoronavirus[MESH] |Acute Lung Injury/*drug therapy/*etiology/immunology[MESH] |COVID-19[MESH] |COVID-19 Drug Treatment[MESH] |Coronavirus Infections/*complications/*drug therapy/immunology[MESH] |Extracellular Traps/*drug effects/immunology[MESH] |Feedback, Physiological[MESH] |Humans[MESH] |Inflammasomes/immunology[MESH] |Interleukin-1beta/*antagonists & inhibitors/immunology[MESH] |Models, Biological[MESH] |NLR Family, Pyrin Domain-Containing 3 Protein/immunology[MESH] |Pandemics[MESH] |Pneumonia, Viral/*complications/*drug therapy/immunology[MESH]Novel therapeutic targets for SARS-CoV-2-induced acute lung injury: Ta(epmc).pdf DeepDyve Pubget Overpricing