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10.1016/j.jbior.2021.100820 http://scihub22266oqcxt.onion/10.1016/j.jbior.2021.100820 34419773!8359569!34419773     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Adv+Biol+Regul 2021 ; 81 (ä): 100820 Nephropedia Template TP {{tp|p=34419773|t=2021. Which ones, when and why should renin-angiotensin system inhibitors work against COVID-19?|pdf=|usr=}}{{34419773}} gab.com Text Which ones, when and why should renin-angiotensin system inhibitors work against COVID-19 JO: Adv Biol Regul http://www.kidney.de/pget.php?&tw=1&pmid=34419773 #FOAvip The article describes the possible pathophysiological origin of COVID-19 and the crucial role of renin-angiotensin system (RAS), providing several "converging" evidence in support of this hypothesis. SARS-CoV-2 has been shown to initially upregulate ACE2 systemic activity (early phase), which can subsequently induce compensatory responses leading to upregulation of both arms of the RAS (late phase) and consequently to critical, advanced and untreatable stages of COVID-19 disease. The main and initial actors of the process are ACE2 and ADAM17 zinc-metalloproteases, which, initially triggered by SARS-CoV-2 spike proteins, work together in increasing circulating Ang 1-7 and Ang 1-9 peptides and downstream (Mas and Angiotensin type 2 receptors) pathways with anti-inflammatory, hypotensive and antithrombotic activities. During the late phase of severe COVID-19, compensatory secretion of renin and ACE enzymes are subsequently upregulated, leading to inflammation, hypertension and thrombosis, which further sustain ACE2 and ADAM17 upregulation. Based on this hypothesis, COVID-19-phase-specific inhibition of different RAS enzymes is proposed as a pharmacological strategy against COVID-19 and vaccine-induced adverse effects. The aim is to prevent the establishment of positive feedback-loops, which can sustain hyperactivity of both arms of the RAS independently of viral trigger and, in some cases, may lead to Long-COVID syndrome. Twit Text FOAVip Which ones, when and why should renin-angiotensin system inhibitors work against COVID-19 ????Adv Biol Regul http://www.kidney.de/pget.php?&tw=1&pmid=34419773 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34419773 #FOAvip English Wikipedia <ref>{{Cite pmid|34419773}}</ref> Which ones, when and why should renin-angiotensin system inhibitors work against COVID-19? #MMPMID34419773 Montanari M; Canonico B; Nordi E; Vandini D; Barocci S; Benedetti S; Carlotti E; Zamai L Adv Biol Regul 2021[Aug]; 81 (ä): 100820 PMID34419773show ga The article describes the possible pathophysiological origin of COVID-19 and the crucial role of renin-angiotensin system (RAS), providing several "converging" evidence in support of this hypothesis. SARS-CoV-2 has been shown to initially upregulate ACE2 systemic activity (early phase), which can subsequently induce compensatory responses leading to upregulation of both arms of the RAS (late phase) and consequently to critical, advanced and untreatable stages of COVID-19 disease. The main and initial actors of the process are ACE2 and ADAM17 zinc-metalloproteases, which, initially triggered by SARS-CoV-2 spike proteins, work together in increasing circulating Ang 1-7 and Ang 1-9 peptides and downstream (Mas and Angiotensin type 2 receptors) pathways with anti-inflammatory, hypotensive and antithrombotic activities. During the late phase of severe COVID-19, compensatory secretion of renin and ACE enzymes are subsequently upregulated, leading to inflammation, hypertension and thrombosis, which further sustain ACE2 and ADAM17 upregulation. Based on this hypothesis, COVID-19-phase-specific inhibition of different RAS enzymes is proposed as a pharmacological strategy against COVID-19 and vaccine-induced adverse effects. The aim is to prevent the establishment of positive feedback-loops, which can sustain hyperactivity of both arms of the RAS independently of viral trigger and, in some cases, may lead to Long-COVID syndrome. |*Renin-Angiotensin System[MESH] |ADAM17 Protein/antagonists & inhibitors/*biosynthesis[MESH] |Angiotensin I/metabolism[MESH] |Angiotensin-Converting Enzyme 2/antagonists & inhibitors/*biosynthesis[MESH] |COVID-19 Drug Treatment[MESH] |COVID-19/*metabolism[MESH] |Gene Expression Regulation, Enzymologic[MESH] |Humans[MESH] |Peptide Fragments/metabolism[MESH] |SARS-CoV-2/*metabolism[MESH] |Spike Glycoprotein, Coronavirus/antagonists & inhibitors/*metabolism[MESH]Which ones, when and why should renin-angiotensin system inhibitors wo(epmc).pdf DeepDyve Pubget Overpricing