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<t>ACE2</t> is a key enzyme in the RAS, catalyzing the metabolism of Ang II to Ang(1-7) and Ang I to Ang(1-9). ACE2 also mediates degradation of ACE-catalyzed breakdown products, Des-arg9-Bk (B1R agonist) and Lys-des-arg9-Bk. The net result of ACE2 in these two systems is to counterbalance ACE/Ang II/AT1R and Bradykinin/Des-arg9-Bk/B1R pathways. Through its cellular binding and entry mechanisms, SARS-CoV-2 is proposed to result in a reduction of ACE2, leading to elevations in Ang I and II, and leading to AT1R stimulation, and Des-arg9-Bk leading to B1R stimulation thus exacerbating inflammation, vascular leakage, and pro-fibrotic events. Potential therapeutics include those targeted to angiotensin and bradykinin system related peptides, in addition to peptides targeting the ACE2-viral spike (S) protein interaction
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ACE2 is a key enzyme in the RAS, catalyzing the metabolism of Ang II to Ang(1-7) and Ang I to Ang(1-9). ACE2 also mediates degradation of ACE-catalyzed breakdown products, Des-arg9-Bk (B1R agonist) and Lys-des-arg9-Bk. The net result of ACE2 in these two systems is to counterbalance ACE/Ang II/AT1R and Bradykinin/Des-arg9-Bk/B1R pathways. Through its cellular binding and entry mechanisms, SARS-CoV-2 is proposed to result in a reduction of ACE2, leading to elevations in Ang I and II, and leading to AT1R stimulation, and Des-arg9-Bk leading to B1R stimulation thus exacerbating inflammation, vascular leakage, and pro-fibrotic events. Potential therapeutics include those targeted to angiotensin and bradykinin system related peptides, in addition to peptides targeting the ACE2-viral spike (S) protein interaction

Journal: Molecular Medicine

Article Title: SARS-CoV-2 and interferon blockade

doi: 10.1186/s10020-020-00231-w

Figure Lengend Snippet: ACE2 is a key enzyme in the RAS, catalyzing the metabolism of Ang II to Ang(1-7) and Ang I to Ang(1-9). ACE2 also mediates degradation of ACE-catalyzed breakdown products, Des-arg9-Bk (B1R agonist) and Lys-des-arg9-Bk. The net result of ACE2 in these two systems is to counterbalance ACE/Ang II/AT1R and Bradykinin/Des-arg9-Bk/B1R pathways. Through its cellular binding and entry mechanisms, SARS-CoV-2 is proposed to result in a reduction of ACE2, leading to elevations in Ang I and II, and leading to AT1R stimulation, and Des-arg9-Bk leading to B1R stimulation thus exacerbating inflammation, vascular leakage, and pro-fibrotic events. Potential therapeutics include those targeted to angiotensin and bradykinin system related peptides, in addition to peptides targeting the ACE2-viral spike (S) protein interaction

Article Snippet: Potential therapeutics include those targeted to angiotensin and bradykinin system related peptides, in addition to peptides targeting the ACE2-viral spike (S) protein interaction Several candidate therapeutics focus on the virus, targeting viral replication (remdesivir), viral entry (Arbidol, APN01, convalescent plasma, monoclonal antibodies (REGN-COV2), camostat mesylate), or critical viral proteins (protease inhibitors).

Techniques: Binding Assay