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ACE2 lowers blood pressure by catalysing the cleavage of the peptide "angiotensin II" (a vasoconstrictor) into angiotensin 1–7 (a vasodilator).

As a transmembrane protein, ACE2 serves as the main entry point into cells for some coronaviruses, including HCoV-NL63, SARS-CoV, the virus that causes SARS, and SARS-CoV-2, the virus that causes COVID-19. This might lead some to believe that decreasing the levels of ACE2, in cells, might help in fighting the infection. On the other hand, ACE2 has been shown to have a protective effect against virus-induced lung injury by increasing the production of the vasodilator angiotensin 1–7. 

Both ACE inhibitors and angiotensin receptor blockers (ARBs) that are used to treat high blood pressure have been shown in a comparative study to upregulate ACE2 expression hence may affect the severity of some other coronavirus infections (e.g., SARS). However, multiple regulatory bodies have recommended continuing standard ACE inhibitors and ARB therapy. A systematic review and meta-analysis found that "use of ACE inhibitors was associated with a significant 34% reduction in risk of pneumonia compared with controls...Use of ACE inhibitors was also associated with a reduction in pneumonia-related mortality, although the results were less robust than for overall risk of pneumonia."

The Angiotensin 1 converting enzyme (ACE) gene codes for the ACE protein and is part of the renin-angiotensin system (RAS), which controls blood pressure by regulating fluid volume in the body.

ACE also contributes to salt sensitivity. An ACE gene polymorphism associated with an increased ACE activity might be associated with the atherosclerotic process and consequently cardiovascular disease and mortality. It also plays a role in your endurance and performance potential, fat cell growth and differentiation, weight gain and obesity, blood sugar balance, and insulin sensitivity. 

When considering your daily health choices, it is important for you to take a polygenic view and consider your genotype for ACTN3, PPARA, PPARGC1A, VEGF, and AGT

Co-enzyme Q10 and zinc are considered to provide co-factor support to this pathway.