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10.1016/j.ejphar.2020.173656 http://scihub22266oqcxt.onion/10.1016/j.ejphar.2020.173656 33086029!7568848!33086029     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       Eur+J+Pharmacol 2021 ; 890 (ä): 173656 Nephropedia Template TP {{tp|p=33086029|t=2021. Renin-angiotensin system at the interface of COVID-19 infection |pdf=|usr=}}{{33086029}} gab.com Text Renin-angiotensin system at the interface of COVID-19 infection JO: Eur J Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=33086029 #FOAvip Angiotensin-converting enzyme 2 (ACE2) has been recognized as a potential entry receptor for SARS-CoV-2 infection. Binding of SARS-CoV-2 to ACE2 allows engagement with pulmonary epithelial cells and pulmonary infection with the virus. ACE2 is an essential component of renin-angiotensin system (RAS), and involved in promoting protective effects to counter-regulate angiotensin (Ang) II-induced pathogenesis. The use of angiotensin receptor blockers (ARBs) and ACE inhibitors (ACEIs) was implicitly negated during the early phase of COVID-19 pandemic, considering the role of these antihypertensive agents in enhancing ACE2 expression thereby promoting the susceptibility to SARS-CoV-2. However, no clinical data has supported this assumption, but indeed evidence demonstrates that ACEIs and ARBs, besides their cardioprotective effects in COVID-19 patients with cardiovascular diseases, might also be beneficial in acute lung injuries by preserving the ACE2 function and switching the balance from deleterious ACE/Ang II/AT(1) receptor axis towards a protective ACE2/Ang (1-7)/Mas receptor axis. Twit Text FOAVip Renin-angiotensin system at the interface of COVID-19 infection ????Eur J Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=33086029 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33086029 #FOAvip English Wikipedia <ref>{{Cite pmid|33086029}}</ref> Renin-angiotensin system at the interface of COVID-19 infection #MMPMID33086029 Gul R; Kim UH; Alfadda AA Eur J Pharmacol 2021[Jan]; 890 (ä): 173656 PMID33086029show ga Angiotensin-converting enzyme 2 (ACE2) has been recognized as a potential entry receptor for SARS-CoV-2 infection. Binding of SARS-CoV-2 to ACE2 allows engagement with pulmonary epithelial cells and pulmonary infection with the virus. ACE2 is an essential component of renin-angiotensin system (RAS), and involved in promoting protective effects to counter-regulate angiotensin (Ang) II-induced pathogenesis. The use of angiotensin receptor blockers (ARBs) and ACE inhibitors (ACEIs) was implicitly negated during the early phase of COVID-19 pandemic, considering the role of these antihypertensive agents in enhancing ACE2 expression thereby promoting the susceptibility to SARS-CoV-2. However, no clinical data has supported this assumption, but indeed evidence demonstrates that ACEIs and ARBs, besides their cardioprotective effects in COVID-19 patients with cardiovascular diseases, might also be beneficial in acute lung injuries by preserving the ACE2 function and switching the balance from deleterious ACE/Ang II/AT(1) receptor axis towards a protective ACE2/Ang (1-7)/Mas receptor axis. |*COVID-19 Drug Treatment[MESH] |*Renin-Angiotensin System[MESH] |*SARS-CoV-2/physiology[MESH] |Angiotensin Receptor Antagonists/*therapeutic use[MESH] |Angiotensin-Converting Enzyme 2/metabolism[MESH] |Angiotensin-Converting Enzyme Inhibitors/*therapeutic use[MESH] |Animals[MESH] |COVID-19/metabolism[MESH] |Humans[MESH] |Proto-Oncogene Mas[MESH] |Proto-Oncogene Proteins/metabolism[MESH] |Receptors, G-Protein-Coupled/metabolism[MESH] |Severe Acute Respiratory Syndrome[MESH]Renin-angiotensin system at the interface of COVID-19 infection (epmc).pdf DeepDyve Pubget Overpricing