Sandbox Reserved 1849: Difference between revisions

<scene name='10/1075251/Ace2/3'>ACE2</scene> (PDB: [https://www.rcsb.org/structure/1R4L 1R4L]) is a carboxypeptidase present on cell surfaces that is responsible for the degradation of angiotensin II. It is a critical enzyme in the suppression of the renin-angiotensin system. This improves both cardiovascular and renal systems, as well as abates acute respiratory distress syndrome (ARDS). It does the 2 former via the RAS System's role in the regulation of blood pressure, renal function, water homeostasis, electrolyte balance, and/or inflammation<ref name="Kuba ACE2-SARS Pathogenesis">PMID:35003058</ref>. The critical role that this enzyme plays in the regulation of this system is what results in the adverse symptomology observed in victims of the SARS-COV-2 virus. The ACE2 receptor is considered the only essential receptor in the SARS-COV-2 viral mechanism, and thus the collateral debilitation of ACE2 results in the adverse respiratory effects including ARDS, pulmonary edema, destruction of alveolar structures, and others<ref name="Kuba ACE2-SARS Pathogenesis">PMID:35003058</ref>. This relationship was further proven when ACE-2 deficient mice had developed these effects at higher rates compared to the wild type<ref name="Kuba Lung Injury">PMID:16007097</ref>. Further information can be found in [[Angiotensin-Converting_Enzyme]]