Preprint Brief Report Version 3 This version is not peer-reviewed

Yin-Yang Balance of ACE/ACE2 Pathways: The Rational for Administration of ACE2 Pathway Inhibitors in Patients Infected by SARS-CoV-2

Version 1 : Received: 19 March 2020 / Approved: 23 March 2020 / Online: 23 March 2020 (06:29:42 CET)
Version 2 : Received: 23 March 2020 / Approved: 24 March 2020 / Online: 24 March 2020 (06:47:18 CET)
Version 3 : Received: 5 May 2020 / Approved: 6 May 2020 / Online: 6 May 2020 (04:40:25 CEST)

A peer-reviewed article of this Preprint also exists.

Zamai, L. The Yin and Yang of ACE/ACE2 Pathways: The Rationale for the Use of Renin-Angiotensin System Inhibitors in COVID-19 Patients. Cells 2020, 9, 1704. Zamai, L. The Yin and Yang of ACE/ACE2 Pathways: The Rationale for the Use of Renin-Angiotensin System Inhibitors in COVID-19 Patients. Cells 2020, 9, 1704.

Journal reference: Cells 2020, 9
DOI: 10.3390/cells9071704

Abstract

The article describes the rational for inhibition of the angiotensin-converting enzyme 2 (ACE2) pathways as specific targets in patients infected by SARS-CoV-2 in order to prevent the establishment of positive feedback loops triggered by COVID-19 in some predisposed subjects. Making use of a large quantity of published reports in which human/rodent ACE2 pathway inhibitors were administered in vivo, it is hypothesized a possible therapeutic pharmacological intervention through an inhibition strategy of the zinc metalloprotease ACE2 and its downstream pathway for SARS-CoV-2 patients. Of even more interest, metal (zinc) chelators and renin inhibitors (both FDA approved drugs) may also work alone or in combination in inhibiting the positive feedback loops, initially triggered by COVID-19 and subsequently sustained by hypoxia independently on viral trigger, when both arms of renin-angiotensin system (ACE2 and ACE) are upregulated, leading to critical, advanced and untreatable stages of the disease.

Supplementary and Associated Material

Subject Areas

Severe Acute Respiratory Syndrome Coronavirus-2; (soluble) ACE2; eosinophil; asthma; IL-10; Lung fibrosis; hypercapnic acidosis; hypoxia; infarction; hypertension; cardiac dysfunction; respiratory distress; coagulopathy; Angiotensin; renin; Ang (1-7); Ang (1-9); Mas receptor; AT2 receptor

Comments (1)

Comment 1
Received: 6 May 2020
Commenter: Loris ZAMAI
Commenter's Conflict of Interests: Author
Comment: Manuscript was improved with more sections regarding different aspects of COVID-19
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