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10.3390/cells9071652 http://scihub22266oqcxt.onion/10.3390/cells9071652 32660065!7407648!32660065     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       Cells 2020 ; 9 (7): ä Nephropedia Template TP {{tp|p=32660065|t=2020. COVID-19, Renin-Angiotensin System and Endothelial Dysfunction |pdf=|usr=}}{{32660065}} gab.com Text COVID-19, Renin-Angiotensin System and Endothelial Dysfunction JO: Cells http://www.kidney.de/pget.php?&tw=1&pmid=32660065 #FOAvip The newly emergent novel coronavirus disease 2019 (COVID-19) outbreak, which is caused by SARS-CoV-2 virus, has posed a serious threat to global public health and caused worldwide social and economic breakdown. Angiotensin-converting enzyme 2 (ACE2) is expressed in human vascular endothelium, respiratory epithelium, and other cell types, and is thought to be a primary mechanism of SARS-CoV-2 entry and infection. In physiological condition, ACE2 via its carboxypeptidase activity generates angiotensin fragments (Ang 1-9 and Ang 1-7), and plays an essential role in the renin-angiotensin system (RAS), which is a critical regulator of cardiovascular homeostasis. SARS-CoV-2 via its surface spike glycoprotein interacts with ACE2 and invades the host cells. Once inside the host cells, SARS-CoV-2 induces acute respiratory distress syndrome (ARDS), stimulates immune response (i.e., cytokine storm) and vascular damage. SARS-CoV-2 induced endothelial cell injury could exacerbate endothelial dysfunction, which is a hallmark of aging, hypertension, and obesity, leading to further complications. The pathophysiology of endothelial dysfunction and injury offers insights into COVID-19 associated mortality. Here we reviewed the molecular basis of SARS-CoV-2 infection, the roles of ACE2, RAS signaling, and a possible link between the pre-existing endothelial dysfunction and SARS-CoV-2 induced endothelial injury in COVID-19 associated mortality. We also surveyed the roles of cell adhesion molecules (CAMs), including CD209L/L-SIGN and CD209/DC-SIGN in SARS-CoV-2 infection and other related viruses. Understanding the molecular mechanisms of infection, the vascular damage caused by SARS-CoV-2 and pathways involved in the regulation of endothelial dysfunction could lead to new therapeutic strategies against COVID-19. Twit Text FOAVip COVID-19, Renin-Angiotensin System and Endothelial Dysfunction ????Cells http://www.kidney.de/pget.php?&tw=1&pmid=32660065 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32660065 #FOAvip English Wikipedia <ref>{{Cite pmid|32660065}}</ref> COVID-19, Renin-Angiotensin System and Endothelial Dysfunction #MMPMID32660065 Amraei R; Rahimi N Cells 2020[Jul]; 9 (7): ä PMID32660065show ga The newly emergent novel coronavirus disease 2019 (COVID-19) outbreak, which is caused by SARS-CoV-2 virus, has posed a serious threat to global public health and caused worldwide social and economic breakdown. Angiotensin-converting enzyme 2 (ACE2) is expressed in human vascular endothelium, respiratory epithelium, and other cell types, and is thought to be a primary mechanism of SARS-CoV-2 entry and infection. In physiological condition, ACE2 via its carboxypeptidase activity generates angiotensin fragments (Ang 1-9 and Ang 1-7), and plays an essential role in the renin-angiotensin system (RAS), which is a critical regulator of cardiovascular homeostasis. SARS-CoV-2 via its surface spike glycoprotein interacts with ACE2 and invades the host cells. Once inside the host cells, SARS-CoV-2 induces acute respiratory distress syndrome (ARDS), stimulates immune response (i.e., cytokine storm) and vascular damage. SARS-CoV-2 induced endothelial cell injury could exacerbate endothelial dysfunction, which is a hallmark of aging, hypertension, and obesity, leading to further complications. The pathophysiology of endothelial dysfunction and injury offers insights into COVID-19 associated mortality. Here we reviewed the molecular basis of SARS-CoV-2 infection, the roles of ACE2, RAS signaling, and a possible link between the pre-existing endothelial dysfunction and SARS-CoV-2 induced endothelial injury in COVID-19 associated mortality. We also surveyed the roles of cell adhesion molecules (CAMs), including CD209L/L-SIGN and CD209/DC-SIGN in SARS-CoV-2 infection and other related viruses. Understanding the molecular mechanisms of infection, the vascular damage caused by SARS-CoV-2 and pathways involved in the regulation of endothelial dysfunction could lead to new therapeutic strategies against COVID-19. |*Renin-Angiotensin System[MESH] |Angiotensin I/metabolism[MESH] |Angiotensin-Converting Enzyme 2[MESH] |Betacoronavirus/isolation & purification[MESH] |COVID-19[MESH] |Cell Adhesion Molecules/metabolism[MESH] |Coronavirus Infections/metabolism/*pathology/virology[MESH] |Endothelium, Vascular/*metabolism[MESH] |Host Microbial Interactions[MESH] |Humans[MESH] |Pandemics[MESH] |Peptidyl-Dipeptidase A/metabolism[MESH] |Pneumonia, Viral/metabolism/*pathology/virology[MESH] |SARS-CoV-2[MESH]COVID-19, Renin-Angiotensin System and Endothelial Dysfunction (epmc).pdf DeepDyve Pubget Overpricing