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. 2020 Apr 28;95(7):1354–1368. doi: 10.1016/j.mayocp.2020.04.028

Figure 4.

Figure 4

Angiotensin-converting enzyme type 2 (ACE2) overexpression and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Central illustration shows possible mechanism behind ACE2 overexpression and SARS-CoV-2 infection picturing normal ACE2 expression (left) and ACE2 protein overexpression in obstructive hypertrophic cardiomyopathy (HCM; right). The SARS-CoV-2 virus hijacks membrane-bound ACE2 for cellular entry. Aside from allowing cellular invasion and viral replication, internalization of the SARS-CoV-2–ACE2 complex causes a decrease in surface ACE2. Loss of surface ACE2: (1) increases the angiotensin II to ang (1-7) ratio and (2) increases angiotensin type 1 receptor (AT1R) activity with a resultant increase in damaging angiotensin II activity. Shown are potential therapeutic targets (and clinical trials) using either angiotensin receptor blockers (ARBs; losartan specifically) or human recombinant soluble ACE2 (hrsACE2). For patients with ACE2-accentuating heart diseases such as obstructive HCM, the speculated increase in viral infectivity of the heart muscle remains to be proven. (Portion of figure adapted from: Simmons G, Zmora P, Gierer S, Heurich A, Pöhlman S. Proteolytic activation of the SARS-coronavirus spike protein: Cutting enzymes at the cutting edge of antiviral research. Antivir Res. 2013;100(3):605-614 with permission from Elsevier, license number 4814880904484).