ACE2 is a surface bound enzyme, but when mice neuro-2A cells were exposed to Ang II and AT1R was activated, ACE2 was removed from the surface of the cell and degraded by lysosomes.  This may be a relevant mechanism related to SARS-CoV-2 cell entry.  

Neuronal ACE2 Internalization in COVID-19

When activated by Ang II, this receptor results in the following physiological outcomes:

- vasoconstriction

- inflammation

- reabsorption of salts and water

- oxidative stress, accelerated aging and brain degeneration

- kidney failure

- heart disease

- apoptosis


Syracuse University

Michigan State University

Ang II is the produce of Ang I being cleaved by ACE.  This molecule is considered biologically active because it can influence physiological outcomes by acting on either Ang II type 1 receptors (AT1R) or Ang type 2 (AT2R) receptors.  

Angiotensin II (Ang II)

Patel, V. B., Zhong, J. C., Grant, M. B., & Oudit, G. Y. (2016). Role of the ACE2/angiotensin 1–7 axis of the renin–angiotensin system in heart failure. Circulation research, 118(8), 1313-1326.

Role of the ACE2/Angiotensin 1–7 axis of the Renin-Angiotensin System in Heart Failure

Ang II type 1 receptors (AT1R)

A receptor that is activated by Ang II.  

Ang II type 2 receptors (AT2R)

ACE2 is a homologue of ACE.  Both enzymes are carboxypeptidases, meaning they cleave amino acids from the c-terminal of the peptide.  However, these homologues cleave the amino acid sequences at different points which leads to their different products.  ACE2 has four main physiological roles:

- Regulating blood pressure via its role in the renin-angiotensin-aldosterone system (RAAS)

- Limiting the amount of ACE substrate by converting Ang I into Ang 1-9

- Degrading Ang II in order to minimize its harmful effects

- Forming Ang 1-7 in order to maximize its cardioprotective effects

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