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        The angiotensin-converting enzyme 2 (ACE2) receptor in the prevention and treatment of COVID-19 are distinctly different paradigms

        McLachlan Craig Steven 대한고혈압학회 2020 Clinical Hypertension Vol.26 No.4

        There is current debate concerning the use of angiotensin-converting enzyme (ACE) inhibitors or angiotensin II type 1 receptor blockers (ARBs), for hypertension management, during COVID-19 infection. Specifically, the suggestion has been made that ACE inhibitors or ARBs could theoretically contribute to infection via increasing ACE2 receptor expression and hence increase viral load. The ACE2 receptor is responsible for binding the SAR-CoV2 viral spike and causing COVID-19 infection. What makes the argument somewhat obtuse for ACE inhibitors or ARBs is that ACE2 receptor expression can be increased by compounds that activate or increase the expression of SIRT1. Henceforth common dietary interventions, vitamins and nutrients may directly or indirectly influence the cellular expression of the ACE2 receptor. There are many common compounds that can increase the expression of the ACE2 receptor including Vitamin C, Metformin, Resveratrol, Vitamin B3 and Vitamin D. It is important to acknowledge that down-regulation or blocking the cellular ACE2 receptor will likely be pro-inflammatory and may contribute to end organ pathology and mortality in COVID-19. In conclusion from the perspective of the ACE2 receptor, COVID-19 prevention and treatment are distinctly different. This letter reflects on this current debate and suggests angiotensin-converting enzyme inhibitors and ARBs are likely beneficial during COVID-19 infection for hypertensive and normotensive patients.

      • Relationship Between ACE Insertion/Deletion Genotype, Telomere Length and Diabetes Mellitus Type Ii

        ( Yu Ling Zhou ),( Ya Xin Lu ),( Herbert Jelinek ),( Hassan Assareh ),( Craig S Mclachlan ),( Brett D Hambly ) 대한내과학회 2014 대한내과학회 추계학술대회 Vol.2014 No.1

        Background: Telomere length has been used as a surrogate biomarker for biological aging. Chronic diseases, i.e. Type 2 Diabetes mellitus (DMT2), resulting in infl ammation have been reported to shorten telomere length. The deletion allele of the angiotensin- converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism has been associated with infl ammation and susceptibility and severity of DMT2. We aimed to examine the interactions of ACE I/D genotype and DMT2 on telomere length. Methods: A total of 195 healthy controls and 80 patients with DMT2 were recruited from the Charles Sturt University Diabetes Screening Research Initiative in Australia. We measured leukocyte telomere length (LTL) by monochrome multiplex quantitative PCR and genotyped ACE I/D polymorphism by PCR and electrophoresis. Multivariate linear regression was used to determine the relationship between telomere length and ACE I/D genotype, covariates controlled for diabetic status. Results: Total population data demonstrated ACE DD or ID genotype carriers have longer mean LTL (1.091 and 1.095, respectively) than II genotype carriers (1.063, P=0.036). When stratifi ed on the basis of diabetes or no diabetes, a signifi cant increase in LTL was maintained in control subjects, but not in the DMT2 subjects. In control subjects, mean relative LTL for DD plus ID carriers is 1.090 and II carriers is 1.043 (P=0.009). In DMT2 patients, the mean relative LTL of samples carrying at least one D allele is 1.089 and II genotype carriers is 1.083 (P=0.868). In control but not DMT2 patients, female gender is associated with longer relative LTL (1.103, P=0.010). Conclusions: The II genotype is associated with shorter telomere length in a control population, but this association is lost in DMT2 patients. These findings support a hypothesis that ACE DD or ID genotype increases telomere length but that diabetes mellitus status alters this effect.

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