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. 2020 Jun;35(3):256-258.
doi: 10.1007/s12250-020-00205-6. Epub 2020 Feb 7.

Compensation of ACE2 Function for Possible Clinical Management of 2019-nCoV-Induced Acute Lung Injury

Yuntao Wu  1
Affiliations

Compensation of ACE2 Function for Possible Clinical Management of 2019-nCoV-Induced Acute Lung Injury

Yuntao Wu. Virol Sin. 2020 Jun.
No abstract available

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Conflict of interest statement

The authors declare that they have no conflict of interest.

Figures

Fig. 1
Fig. 1
Potential therapeutics for 2019-nCoV-induced lung injury based on balancing the renin–angiotensin system (RAS). Activation of the RAS cascade involves Renin cleaves angiotensinogen to generate Ang I, which is then converted to Ang II by ACE. Ang II binds to its receptors (AT1 and AT2) to exert local and systemic effects such as vasoconstriction and promotion of the release of aldosterone. ACE2 functions as a counter-regulatory enzyme for balancing responses initiated from ACE. ACE2 hydrolyses Ang I and Ang II to generate Ang-(1–9) and Ang-(1–7). Ang-(1–7) binding to the MAS receptor antagonizes Ang II-mediated actions. SARS-CoV and 2019-nCoV use ACE2 as the entry receptor. Inhibition of ACE2 expression or downregulation of surface ACE2 by these coronaviruses may disrupt function balances between ACE/ACE2, which may be alleviated by different approaches (from A to D).
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