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10.3389/fimmu.2022.838011 http://scihub22266oqcxt.onion/10.3389/fimmu.2022.838011 35309344!8924116!35309344     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Front+Immunol 2022 ; 13 (ä): 838011 Nephropedia Template TP {{tp|p=35309344|t=2022. NETosis and Neutrophil Extracellular Traps in COVID-19: Immunothrombosis and Beyond |pdf=|usr=}}{{35309344}} gab.com Text NETosis and Neutrophil Extracellular Traps in COVID-19: Immunothrombosis and Beyond JO: Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=35309344 #FOAvip Infection with SARS-CoV-2, the causative agent of the Coronavirus disease 2019 (COVID-19) pandemic, causes respiratory problems and multifaceted organ dysfunction. A crucial mechanism of COVID-19 immunopathy is the recruitment and activation of neutrophils at the infection site, which also predicts disease severity and poor outcomes. The release of neutrophil extracellular traps (NETs), occurring during a regulated form of neutrophil cell death known as NETosis, is a key effector function that mediates harmful effects caused by neutrophils. Abundant NETosis and NET generation have been observed in the neutrophils of many COVID-19 patients, leading to unfavorable coagulopathy and immunothrombosis. Moreover, excessive NETosis and NET generation are now more widely recognized as mediators of additional pathophysiological abnormalities following SARS-CoV-2 infection. In this minireview, we introduce subtypes of NET-producing neutrophils (e.g., low-density granulocytes) and explain the biological importance of NETs and the protein cargos of NETs in COVID-19. In addition, we discuss the mechanisms by which SARS-CoV-2 causes NETosis by upregulating viral processes (e.g., viral entry and replication) as well as host pro-NET mechanisms (e.g., proinflammatory mediator release, platelet activation, and autoantibody production). Furthermore, we provide an update of the main findings of NETosis and NETs in immunothrombosis and other COVID-19-related disorders, such as aberrant immunity, neurological disorders, and post COVID-19 syndromes including lung fibrosis, neurological disorder, tumor progression, and deteriorated chronic illness. Finally, we address potential prospective COVID-19 treatment strategies that target dysregulated NETosis and NET formation via inhibition of NETosis and promotion of NET degradation, respectively. Twit Text FOAVip NETosis and Neutrophil Extracellular Traps in COVID-19: Immunothrombosis and Beyond ????Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=35309344 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=35309344 #FOAvip English Wikipedia <ref>{{Cite pmid|35309344}}</ref> NETosis and Neutrophil Extracellular Traps in COVID-19: Immunothrombosis and Beyond #MMPMID35309344 Zhu Y; Chen X; Liu X Front Immunol 2022[]; 13 (ä): 838011 PMID35309344show ga Infection with SARS-CoV-2, the causative agent of the Coronavirus disease 2019 (COVID-19) pandemic, causes respiratory problems and multifaceted organ dysfunction. A crucial mechanism of COVID-19 immunopathy is the recruitment and activation of neutrophils at the infection site, which also predicts disease severity and poor outcomes. The release of neutrophil extracellular traps (NETs), occurring during a regulated form of neutrophil cell death known as NETosis, is a key effector function that mediates harmful effects caused by neutrophils. Abundant NETosis and NET generation have been observed in the neutrophils of many COVID-19 patients, leading to unfavorable coagulopathy and immunothrombosis. Moreover, excessive NETosis and NET generation are now more widely recognized as mediators of additional pathophysiological abnormalities following SARS-CoV-2 infection. In this minireview, we introduce subtypes of NET-producing neutrophils (e.g., low-density granulocytes) and explain the biological importance of NETs and the protein cargos of NETs in COVID-19. In addition, we discuss the mechanisms by which SARS-CoV-2 causes NETosis by upregulating viral processes (e.g., viral entry and replication) as well as host pro-NET mechanisms (e.g., proinflammatory mediator release, platelet activation, and autoantibody production). Furthermore, we provide an update of the main findings of NETosis and NETs in immunothrombosis and other COVID-19-related disorders, such as aberrant immunity, neurological disorders, and post COVID-19 syndromes including lung fibrosis, neurological disorder, tumor progression, and deteriorated chronic illness. Finally, we address potential prospective COVID-19 treatment strategies that target dysregulated NETosis and NET formation via inhibition of NETosis and promotion of NET degradation, respectively. |Animals[MESH] |Apoptosis[MESH] |Blood Coagulation Disorders/*immunology[MESH] |COVID-19/*immunology[MESH] |Carcinogenesis[MESH] |Extracellular Traps/*immunology[MESH] |Fibrosis[MESH] |Humans[MESH] |Lung/*pathology[MESH] |Neutrophils/*immunology[MESH] |SARS-CoV-2/*physiology[MESH]NETosis and Neutrophil Extracellular Traps in COVID-19: Immunothrombos(epmc).pdf DeepDyve Pubget Overpricing