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10.5937/jomb0-30659 http://scihub22266oqcxt.onion/10.5937/jomb0-30659 35291496!8882013!35291496     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 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 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Med+Biochem 2022 ; 41 (1): 14-20 Nephropedia Template TP {{tp|p=35291496|t=2022. SARS-CoV-2 infecting endothelial cells, biochemical alterations, autopsy findings and outcomes in COVID-19, suggest role of hypoxia-inducible factor-1 |pdf=|usr=}}{{35291496}} gab.com Text SARS-CoV-2 infecting endothelial cells, biochemical alterations, autopsy findings and outcomes in COVID-19, suggest role of hypoxia-inducible factor-1 JO: J Med Biochem http://www.kidney.de/pget.php?&tw=1&pmid=35291496 #FOAvip Researchers around the world have experienced the dual nature of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), 'tragically lethal in some people while surprisingly benign in others'. There have been congregating studies of the novel coronavirus disease (COVID-19), a disease that mainly attacks the lungs but also has mystifying effects on the heart, kidneys and brain. Researchers are also gathering information to ascertain why people are dying of COVID-19, whether it is solely a respiratory disorder, a coagulation disorder or multi-organ failure. Alterations in laboratory parameters like lactate, ferritin and albumin have been established as risk factors and are associated with outcomes, yet none have not been sub stantiated with a scientific biochemical rationale. SARSCoV-2 affects the alveolar type II epithelial cells which significantly disturbs its surfactant homeostasis, deprives Na,K-ATPase of ATP, thereby disturbing the alveolar lining fluid which then gradually decreases the alveolar gaseous exchange initiating the intracellular hypoxic conditions. This activates AMP-activated kinase, which further inhibits Na,K-ATPase, which can progressively cause respiratory distress syndrome. The virus may infect endothelial cell (EC) which, being less energetic, cannot withstand the huge energy requirement towards viral replication. There - fore glycolysis, the prime energy generating pathway, must be mandatorily upregulated. This can be achieved by Hypoxia-inducible factor-1 (HIF-1). However, HIF-1 also activates transcription of von Willebrand factor, plasminogen activator inhibitor-1, and suppresses the release of thrombomodulin. This in turn sets off the coagulation cascade that can lead to in-situ pulmonary thrombosis and micro clots. The proposed HIF-1 hypothesis justifies various features, biochemical alteration, laboratory as well as autopsy findings such as respiratory distress syndrome, increased blood ferritin and lactate levels, hypoalbuminemia, endothelial invasion, in-situ pulmonary thrombosis and micro clots, and multi-organ failure in COVID-19. Twit Text FOAVip SARS-CoV-2 infecting endothelial cells, biochemical alterations, autopsy findings and outcomes in COVID-19, suggest role of hypoxia-inducible factor-1 ????J Med Biochem http://www.kidney.de/pget.php?&tw=1&pmid=35291496 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=35291496 #FOAvip English Wikipedia <ref>{{Cite pmid|35291496}}</ref> SARS-CoV-2 infecting endothelial cells, biochemical alterations, autopsy findings and outcomes in COVID-19, suggest role of hypoxia-inducible factor-1 #MMPMID35291496 Ambade V; Ambade S J Med Biochem 2022[Feb]; 41 (1): 14-20 PMID35291496show ga Researchers around the world have experienced the dual nature of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), 'tragically lethal in some people while surprisingly benign in others'. There have been congregating studies of the novel coronavirus disease (COVID-19), a disease that mainly attacks the lungs but also has mystifying effects on the heart, kidneys and brain. Researchers are also gathering information to ascertain why people are dying of COVID-19, whether it is solely a respiratory disorder, a coagulation disorder or multi-organ failure. Alterations in laboratory parameters like lactate, ferritin and albumin have been established as risk factors and are associated with outcomes, yet none have not been sub stantiated with a scientific biochemical rationale. SARSCoV-2 affects the alveolar type II epithelial cells which significantly disturbs its surfactant homeostasis, deprives Na,K-ATPase of ATP, thereby disturbing the alveolar lining fluid which then gradually decreases the alveolar gaseous exchange initiating the intracellular hypoxic conditions. This activates AMP-activated kinase, which further inhibits Na,K-ATPase, which can progressively cause respiratory distress syndrome. The virus may infect endothelial cell (EC) which, being less energetic, cannot withstand the huge energy requirement towards viral replication. There - fore glycolysis, the prime energy generating pathway, must be mandatorily upregulated. This can be achieved by Hypoxia-inducible factor-1 (HIF-1). However, HIF-1 also activates transcription of von Willebrand factor, plasminogen activator inhibitor-1, and suppresses the release of thrombomodulin. This in turn sets off the coagulation cascade that can lead to in-situ pulmonary thrombosis and micro clots. The proposed HIF-1 hypothesis justifies various features, biochemical alteration, laboratory as well as autopsy findings such as respiratory distress syndrome, increased blood ferritin and lactate levels, hypoalbuminemia, endothelial invasion, in-situ pulmonary thrombosis and micro clots, and multi-organ failure in COVID-19. äSARS-CoV-2 infecting endothelial cells, biochemical alterations, autop(epmc).pdf DeepDyve Pubget Overpricing