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10.7861/clinmed.2020-0252 http://scihub22266oqcxt.onion/10.7861/clinmed.2020-0252 32601125!7539732!32601125     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       Clin+Med+(Lond) 2020 ; 20 (5): e146-e147 Nephropedia Template TP {{tp|p=32601125|t=2020. Potential role of endothelial cell surface ectopic redox complexes in COVID-19 disease pathogenesis |pdf=|usr=}}{{32601125}} gab.com Text Potential role of endothelial cell surface ectopic redox complexes in COVID-19 disease pathogenesis JO: Clin Med (Lond) http://www.kidney.de/pget.php?&tw=1&pmid=32601125 #FOAvip The novel coronavirus infectious disease (COVID-19) has rapidly spread and poses a great challenge to researchers, both in elucidating its pathogenic mechanism and developing effective treatments. It has been recently proposed that COVID-19 is an endothelial disease. Indeed, the COVID-19 virus binds to angiotensin-converting enzyme type 2 (ACE2), which is expressed in endothelial cells. ACE2 could be implicated in the production of reactive oxygen species (ROS) caused by endothelial dysfunction due to viral damage. Consequently, oxidative stress could prime these cells to acquire a pro-thrombotic and pro-inflammatory phenotype, predisposing patients to thromboembolic and vasculitic events and to disseminated intravascular coagulopathy (DIC). This implies a pivotal role played by oxygen in the pathogenetic mechanism of COVID-19 disease, in that its availability would tune the oxidant state and consequent damage. Twit Text FOAVip Potential role of endothelial cell surface ectopic redox complexes in COVID-19 disease pathogenesis ????Clin Med (Lond) http://www.kidney.de/pget.php?&tw=1&pmid=32601125 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32601125 #FOAvip English Wikipedia <ref>{{Cite pmid|32601125}}</ref> Potential role of endothelial cell surface ectopic redox complexes in COVID-19 disease pathogenesis #MMPMID32601125 Panfoli I Clin Med (Lond) 2020[Sep]; 20 (5): e146-e147 PMID32601125show ga The novel coronavirus infectious disease (COVID-19) has rapidly spread and poses a great challenge to researchers, both in elucidating its pathogenic mechanism and developing effective treatments. It has been recently proposed that COVID-19 is an endothelial disease. Indeed, the COVID-19 virus binds to angiotensin-converting enzyme type 2 (ACE2), which is expressed in endothelial cells. ACE2 could be implicated in the production of reactive oxygen species (ROS) caused by endothelial dysfunction due to viral damage. Consequently, oxidative stress could prime these cells to acquire a pro-thrombotic and pro-inflammatory phenotype, predisposing patients to thromboembolic and vasculitic events and to disseminated intravascular coagulopathy (DIC). This implies a pivotal role played by oxygen in the pathogenetic mechanism of COVID-19 disease, in that its availability would tune the oxidant state and consequent damage. |COVID-19[MESH] |Coronavirus Infections/epidemiology/*physiopathology[MESH] |Disease Progression[MESH] |Endothelial Cells/*cytology[MESH] |Endothelium, Vascular/*metabolism[MESH] |Humans[MESH] |Needs Assessment[MESH] |Pandemics[MESH] |Pneumonia, Viral/epidemiology/*physiopathology[MESH] |Risk Assessment[MESH] |Severe Acute Respiratory Syndrome/epidemiology/*physiopathology[MESH]Potential role of endothelial cell surface ectopic redox complexes in (epmc).pdf DeepDyve Pubget Overpricing