Could a specific ACE2 activator drug improve the clinical outcome of SARS-CoV-2? A potential pharmacological insight
Author:
Affiliation:
1. Department of Medicine, Federal University of Parnaíba Delta, Parnaíba, Brazil
2. Biotechnology and Biodiversity Center Research (BIOTEC), Federal University of Parnaíba Delta, Parnaíba, Brazil
Funder
CNPq
Research Foundation for the State of Piauí—FAPEPI
Publisher
Informa UK Limited
Subject
Pharmacology (medical),General Pharmacology, Toxicology and Pharmaceutics,General Medicine
Link
https://www.tandfonline.com/doi/pdf/10.1080/17512433.2020.1798760
Reference37 articles.
1. Angiotensin-converting enzyme 2 is a functional receptor for the SARS coronavirus
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3. SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor
4. TMPRSS2 and ADAM17 Cleave ACE2 Differentially and Only Proteolysis by TMPRSS2 Augments Entry Driven by the Severe Acute Respiratory Syndrome Coronavirus Spike Protein
5. Tumor Necrosis Factor-α Convertase (ADAM17) Mediates Regulated Ectodomain Shedding of the Severe-acute Respiratory Syndrome-Coronavirus (SARS-CoV) Receptor, Angiotensin-converting Enzyme-2 (ACE2)
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