Angiotensin-converting enzyme 2 (ACE2) in COVID-19 and other diseases.
Atemwegs- und Lungenkrankheiten
; 49(4):129-133, 2023.
Article
in German
| EMBASE | ID: covidwho-20242600
ABSTRACT
The coronavirus SARS-CoV-2 was detected in isolates of pneumonia patients in January 2020. The virus cannot multiply extracellularly but requires access to the cells of a host organism. SARS-CoV-2 uses angiotensin-converting enzyme 2 (ACE2) as a receptor, to which it docks with its spikes. ACE2 belongs to the renin angiotensin system (RAS), whose inhibitors have been used for years against high blood pressure. Renin is an endopeptidase that is predominantly formed in the juxtaglomerular apparatus of the kidney and cleaves the decapeptide angiotensin I (Ang I) from angiotensinogen. Through the angiotensin-converting enzyme (ACE), another 2 C-terminal amino acids are removed from Ang I, so that finally the active octapeptide angiotensin II (Ang II) is formed. The biological effect of Ang II via the angiotensin II receptor subtype 1 (AT1-R) consists of vasoconstriction, fibrosis, proliferation, inflammation, and thrombosis formation. ACE2 is a peptidase that is a homolog of ACE. ACE2 is predominantly expressed by pulmonary alveolar epithelial cells in humans and has been detected in arterial and venous endothelial cells. In contrast to the dicarboxy-peptidase ACE, ACE2 is a monocarboxypeptidase that cleaves only one amino acid from the C-terminal end of the peptides. ACE2 can hydrolyze the nonapeptide Ang-(1-9) from the decapeptide Ang I and the heptapeptide Ang-(1-7) from the octapeptide Ang II. Ang-(1-7) acts predominantly antagonistically (vasodilatory, anti-fibrotic, anti-proliferative, anti-inflammatory, anti-thrombogenetically) via the G protein-coupled Mas receptor to the AT1-R-mediated effects of Ang II. In the pathogenesis of COVID-19 infection, it is therefore assumed that there is an imbalance due to overstimulation of the AT1 receptor in conjunction with a weakening of the biological effects of the Mas receptor.Copyright © 2022 Dustri-Verlag Dr. K. Feistle.
angiotensin-converting enzyme 2; AT-1-Receptor; covid-19; Mas receptor; pulmonary diseases; adult; carboxy terminal sequence; cell proliferation; controlled study; coronavirus disease 2019; endothelium cell; enzyme activity; fibrosis; human; human cell; hydrolysis; hypertension; inflammation; juxtaglomerular apparatus; lung alveolus epithelium cell; lung disease; nonhuman; pneumonia; protein expression; protein function; renin angiotensin aldosterone system; review; Severe acute respiratory syndrome coronavirus 2; spike; thrombosis; vasoconstriction; amino acid; angiotensin 1A receptor; angiotensin converting enzyme 2; angiotensin I; angiotensin II; angiotensin receptor; angiotensinogen; dipeptidyl carboxypeptidase; endogenous compound; guanine nucleotide binding protein; nonapeptide; octapeptide; peptidase; proteinase; renin; talfirastide
Full text:
Available
Collection:
Databases of international organizations
Database:
EMBASE
Language:
German
Journal:
Atemwegs- und Lungenkrankheiten
Year:
2023
Document Type:
Article
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