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10.3389/fmed.2020.626796 http://scihub22266oqcxt.onion/10.3389/fmed.2020.626796 33553219!7859652!33553219     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       Front+Med+(Lausanne) 2020 ; 7 (ä): 626796 Nephropedia Template TP {{tp|p=33553219|t=2020. Can GPR4 Be a Potential Therapeutic Target for COVID-19?|pdf=|usr=}}{{33553219}} gab.com Text Can GPR4 Be a Potential Therapeutic Target for COVID-19 JO: Front Med (Lausanne) http://www.kidney.de/pget.php?&tw=1&pmid=33553219 #FOAvip Coronavirus disease 19 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), first emerged in late 2019 and has since rapidly become a global pandemic. SARS-CoV-2 infection causes damages to the lung and other organs. The clinical manifestations of COVID-19 range widely from asymptomatic infection, mild respiratory illness to severe pneumonia with respiratory failure and death. Autopsy studies demonstrate that diffuse alveolar damage, inflammatory cell infiltration, edema, proteinaceous exudates, and vascular thromboembolism in the lung as well as extrapulmonary injuries in other organs represent key pathological findings. Herein, we hypothesize that GPR4 plays an integral role in COVID-19 pathophysiology and is a potential therapeutic target for the treatment of COVID-19. GPR4 is a pro-inflammatory G protein-coupled receptor (GPCR) highly expressed in vascular endothelial cells and serves as a "gatekeeper" to regulate endothelium-blood cell interaction and leukocyte infiltration. GPR4 also regulates vascular permeability and tissue edema under inflammatory conditions. Therefore, we hypothesize that GPR4 antagonism can potentially be exploited to mitigate the hyper-inflammatory response, vessel hyper-permeability, pulmonary edema, exudate formation, vascular thromboembolism and tissue injury associated with COVID-19. Twit Text FOAVip Can GPR4 Be a Potential Therapeutic Target for COVID-19 ????Front Med (Lausanne) http://www.kidney.de/pget.php?&tw=1&pmid=33553219 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33553219 #FOAvip English Wikipedia <ref>{{Cite pmid|33553219}}</ref> Can GPR4 Be a Potential Therapeutic Target for COVID-19? #MMPMID33553219 Yang LV; Oppelt KA; Thomassen MJ; Marie MA; Nik Akhtar S; McCallen JD Front Med (Lausanne) 2020[]; 7 (ä): 626796 PMID33553219show ga Coronavirus disease 19 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), first emerged in late 2019 and has since rapidly become a global pandemic. SARS-CoV-2 infection causes damages to the lung and other organs. The clinical manifestations of COVID-19 range widely from asymptomatic infection, mild respiratory illness to severe pneumonia with respiratory failure and death. Autopsy studies demonstrate that diffuse alveolar damage, inflammatory cell infiltration, edema, proteinaceous exudates, and vascular thromboembolism in the lung as well as extrapulmonary injuries in other organs represent key pathological findings. Herein, we hypothesize that GPR4 plays an integral role in COVID-19 pathophysiology and is a potential therapeutic target for the treatment of COVID-19. GPR4 is a pro-inflammatory G protein-coupled receptor (GPCR) highly expressed in vascular endothelial cells and serves as a "gatekeeper" to regulate endothelium-blood cell interaction and leukocyte infiltration. GPR4 also regulates vascular permeability and tissue edema under inflammatory conditions. Therefore, we hypothesize that GPR4 antagonism can potentially be exploited to mitigate the hyper-inflammatory response, vessel hyper-permeability, pulmonary edema, exudate formation, vascular thromboembolism and tissue injury associated with COVID-19. äCan GPR4 Be a Potential Therapeutic Target for COVID-19?(epmc).pdf DeepDyve Pubget Overpricing