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10.1007/s11033-021-06642-0 http://scihub22266oqcxt.onion/10.1007/s11033-021-06642-0 34392451!8364628!34392451     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Mol+Biol+Rep 2021 ; 48 (9): 6655-6661 Nephropedia Template TP {{tp|p=34392451|t=2021. How SARS-CoV-2 might affect potassium balance via impairing epithelial sodium channels?|pdf=|usr=}}{{34392451}} gab.com Text How SARS-CoV-2 might affect potassium balance via impairing epithelial sodium channels JO: Mol Biol Rep http://www.kidney.de/pget.php?&tw=1&pmid=34392451 #FOAvip Severe acute respiratory syndrome coronaviruses 2 (SARS-CoV-2) is the causative agent of current coronavirus disease 2019 (COVID-19) pandemic. Electrolyte disorders particularly potassium abnormalities have been repeatedly reported as common clinical manifestations of COVID-19. Here, we discuss how SARS-CoV-2 may affect potassium balance by impairing the activity of epithelial sodium channels (ENaC). The first hypothesis could justify the incidence of hypokalemia. SARS-CoV-2 cell entry through angiotensin-converting enzyme 2 (ACE2) may enhance the activity of renin-angiotensin-aldosterone system (RAAS) classical axis and further leading to over production of aldosterone. Aldosterone is capable of enhancing the activity of ENaC and resulting in potassium loss from epithelial cells. However, type II transmembrane serine protease (TMPRSS2) is able to inhibit the ENaC, but it is utilized in the case of SARS-CoV-2 cell entry, therefore the ENaC remains activated. The second hypothesis describe the incidence of hyperkalemia based on the key role of furin. Furin is necessary for cleaving both SARS-CoV-2 spike protein and ENaC subunits. While the furin is hijacked by the virus, the decreased activity of ENaC would be expected, which causes retention of potassium ions and hyperkalemia. Given that the occurrence of hypokalemia is higher than hyperkalemia in COVID-19 patients, the first hypothesis may have greater impact on potassium levels. Further investigations are warranted to determine the exact role of ENaC in SARS-CoV-2 pathogenesis. Twit Text FOAVip How SARS-CoV-2 might affect potassium balance via impairing epithelial sodium channels ????Mol Biol Rep http://www.kidney.de/pget.php?&tw=1&pmid=34392451 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34392451 #FOAvip English Wikipedia <ref>{{Cite pmid|34392451}}</ref> How SARS-CoV-2 might affect potassium balance via impairing epithelial sodium channels? #MMPMID34392451 Noori M; Nejadghaderi SA; Sullman MJM; Carson-Chahhoud K; Ardalan M; Kolahi AA; Safiri S Mol Biol Rep 2021[Sep]; 48 (9): 6655-6661 PMID34392451show ga Severe acute respiratory syndrome coronaviruses 2 (SARS-CoV-2) is the causative agent of current coronavirus disease 2019 (COVID-19) pandemic. Electrolyte disorders particularly potassium abnormalities have been repeatedly reported as common clinical manifestations of COVID-19. Here, we discuss how SARS-CoV-2 may affect potassium balance by impairing the activity of epithelial sodium channels (ENaC). The first hypothesis could justify the incidence of hypokalemia. SARS-CoV-2 cell entry through angiotensin-converting enzyme 2 (ACE2) may enhance the activity of renin-angiotensin-aldosterone system (RAAS) classical axis and further leading to over production of aldosterone. Aldosterone is capable of enhancing the activity of ENaC and resulting in potassium loss from epithelial cells. However, type II transmembrane serine protease (TMPRSS2) is able to inhibit the ENaC, but it is utilized in the case of SARS-CoV-2 cell entry, therefore the ENaC remains activated. The second hypothesis describe the incidence of hyperkalemia based on the key role of furin. Furin is necessary for cleaving both SARS-CoV-2 spike protein and ENaC subunits. While the furin is hijacked by the virus, the decreased activity of ENaC would be expected, which causes retention of potassium ions and hyperkalemia. Given that the occurrence of hypokalemia is higher than hyperkalemia in COVID-19 patients, the first hypothesis may have greater impact on potassium levels. Further investigations are warranted to determine the exact role of ENaC in SARS-CoV-2 pathogenesis. |COVID-19/*metabolism/virology[MESH] |Epithelial Cells/*metabolism/virology[MESH] |Epithelial Sodium Channels/*metabolism[MESH] |Furin/metabolism[MESH] |Humans[MESH] |Pandemics/prevention & control[MESH] |Potassium/*metabolism[MESH] |SARS-CoV-2/*metabolism[MESH] |Serine Endopeptidases/metabolism[MESH]How SARS-CoV-2 might affect potassium balance via impairing epithelial(epmc).pdf DeepDyve Pubget Overpricing