COVID-19: Critical Role of Angiotensin 1-7 in ACE2 Modulation
Ching Siang Tan, Siang Fei Yeoh, Chiau Ming Long
Abstract
With the declaration of Novel Coronavirus Disease 2019 (COVID-19) as pandemic by World Health Organization (WHO), many countries have taken drastic measure to enforce movement control to curb COVID-19 outbreak. On 23 January 2020, it was reported that Malaysia had 4 patients suspected to have contracted the COVID-19. On the same day, Singapore confirmed its first case of COVID-19. To date, WHO has reported a total of 5.6 million confirmed cases, with 353,373 confirmed deaths among 216 countries around the world. imilar to SAR-Cov (Severe Acute Respiratory Syndrome Coronavirus), COVID-19 is believed to be using the same entry point of Angiotensin Converting Enzyme 2 (ACE2) into the human host cells. CE2 is a carboxymonopeptidase that cleaves at the carboxy-terminal (C-terminal) end of a protein or peptide [6], and is expressed on respiratory and intestinal epithelial cells, endothelial cells, renal tubule cells and immune cells. 6-10 Tipnis et al (2000) also reported that the mammalian homologue of ACE has implications on cardiovascular and renal function. 11 Up to 96% of ACE2 is available as membrane-bound enzyme, and the minority of ACE2 (1-4%) presents as a soluble form in blood, urine, and other body fluids. dditionally, the latest study by Wan et al (2020) reported that COVID-19 uses the same receptor-binding motif, as SAR-Cov that directly contacts with ACE2. here is an intrinsically high renin angiotensin system (RAS) activity in the lungs, creating a relatively higher concentration of ACE2 in the organ. Interestingly, Angiotensin Converting Enzyme (ACE) inhibitors, which are commonly prescribed for hypertension treatment, antagonise specifically the effect of ACE, but not ACE2. [15] ACE2 plays an important role in RAS, by converting Angiotensin II to Angiotensin