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10.1111/bph.15082 http://scihub22266oqcxt.onion/10.1111/bph.15082 32333398!7572451!32333398     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=32333398&cmd=llinks): Failed to open stream: HTTP request failed! 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A hypothesis for pathobiology and treatment of COVID-19: The centrality of ACE1/ACE2 imbalance |pdf=|usr=}}{{32333398}} gab.com Text A hypothesis for pathobiology and treatment of COVID-19: The centrality of ACE1/ACE2 imbalance JO: Br J Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=32333398 #FOAvip Angiotensin Converting Enzyme2 is the cell surface binding site for the coronavirus SARS-CoV-2, which causes COVID-19. We propose that an imbalance in the action of ACE1- and ACE2-derived peptides, thereby enhancing angiotensin II (Ang II) signalling is primary driver of COVID-19 pathobiology. ACE1/ACE2 imbalance occurs due to the binding of SARS-CoV-2 to ACE2, reducing ACE2-mediated conversion of Ang II to Ang peptides that counteract pathophysiological effects of ACE1-generated ANG II. This hypothesis suggests several approaches to treat COVID-19 by restoring ACE1/ACE2 balance: (a) AT receptor antagonists; (b) ACE1 inhibitors (ACEIs); (iii) agonists of receptors activated by ACE2-derived peptides (e.g. Ang (1-7), which activates MAS1); (d) recombinant human ACE2 or ACE2 peptides as decoys for the virus. Reducing ACE1/ACE2 imbalance is predicted to blunt COVID-19-associated morbidity and mortality, especially in vulnerable patients. Importantly, approved AT antagonists and ACEIs can be rapidly repurposed to test their efficacy in treating COVID-19. LINKED ARTICLES: This article is part of a themed issue on The Pharmacology of COVID-19. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v177.21/issuetoc. Twit Text FOAVip A hypothesis for pathobiology and treatment of COVID-19: The centrality of ACE1/ACE2 imbalance ????Br J Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=32333398 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32333398 #FOAvip English Wikipedia <ref>{{Cite pmid|32333398}}</ref> A hypothesis for pathobiology and treatment of COVID-19: The centrality of ACE1/ACE2 imbalance #MMPMID32333398 Sriram K; Insel PA Br J Pharmacol 2020[Nov]; 177 (21): 4825-4844 PMID32333398show ga Angiotensin Converting Enzyme2 is the cell surface binding site for the coronavirus SARS-CoV-2, which causes COVID-19. We propose that an imbalance in the action of ACE1- and ACE2-derived peptides, thereby enhancing angiotensin II (Ang II) signalling is primary driver of COVID-19 pathobiology. ACE1/ACE2 imbalance occurs due to the binding of SARS-CoV-2 to ACE2, reducing ACE2-mediated conversion of Ang II to Ang peptides that counteract pathophysiological effects of ACE1-generated ANG II. This hypothesis suggests several approaches to treat COVID-19 by restoring ACE1/ACE2 balance: (a) AT receptor antagonists; (b) ACE1 inhibitors (ACEIs); (iii) agonists of receptors activated by ACE2-derived peptides (e.g. Ang (1-7), which activates MAS1); (d) recombinant human ACE2 or ACE2 peptides as decoys for the virus. Reducing ACE1/ACE2 imbalance is predicted to blunt COVID-19-associated morbidity and mortality, especially in vulnerable patients. Importantly, approved AT antagonists and ACEIs can be rapidly repurposed to test their efficacy in treating COVID-19. LINKED ARTICLES: This article is part of a themed issue on The Pharmacology of COVID-19. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v177.21/issuetoc. |Angiotensin II Type 1 Receptor Blockers/pharmacology[MESH] |Angiotensin-Converting Enzyme 2[MESH] |Angiotensin-Converting Enzyme Inhibitors/pharmacology[MESH] |Animals[MESH] |Betacoronavirus/enzymology/*isolation & purification[MESH] |COVID-19[MESH] |COVID-19 Drug Treatment[MESH] |Coronavirus Infections/*drug therapy/enzymology/virology[MESH] |Drug Repositioning[MESH] |Humans[MESH] |Pandemics[MESH] |Peptidyl-Dipeptidase A/metabolism[MESH] |Pneumonia, Viral/*drug therapy/enzymology/virology[MESH] |Proto-Oncogene Mas[MESH]A hypothesis for pathobiology and treatment of COVID-19: The centralit(epmc).pdf DeepDyve Pubget Overpricing