| Literature DB >> 34359922 |
Christian Zanza1,2,3, Michele Fidel Tassi4, Tatsiana Romenskaya2, Fabio Piccolella2, Ludovico Abenavoli5, Francesco Franceschi1, Andrea Piccioni1, Veronica Ojetti1, Angela Saviano1, Barbara Canonico6, Mariele Montanari6, Loris Zamai6,7, Marco Artico8, Chiara Robba9, Fabrizio Racca2, Yaroslava Longhitano2,3.
Abstract
Since the end of 2019, the medical-scientific community has been facing a terrible pandemic caused by a new airborne viral agent known as SARS-CoV2. Already in the early stages of the pandemic, following the discovery that the virus uses the ACE2 cell receptor as a molecular target to infect the cells of our body, it was hypothesized that the renin-angiotensin-aldosterone system was involved in the pathogenesis of the disease. Since then, numerous studies have been published on the subject, but the exact role of the renin-angiotensin-aldosterone system in the pathogenesis of COVID-19 is still a matter of debate. RAAS represents an important protagonist in the pathogenesis of COVID-19, providing the virus with the receptor of entry into host cells and determining its organotropism. Furthermore, following infection, the virus is able to cause an increase in plasma ACE2 activity, compromising the normal function of the RAAS. This dysfunction could contribute to the establishment of the thrombo-inflammatory state characteristic of severe forms of COVID-19. Drugs targeting RAAS represent promising therapeutic options for COVID-19 sufferers.Entities:
Keywords: ACE inhibitors; ACE2; COVID-19; SARS-CoV2; renin-angiotensin-aldosterone system; sartans; zinc-chelating agents
Year: 2021 PMID: 34359922 DOI: 10.3390/cells10071752
Source DB: PubMed Journal: Cells ISSN: 2073-4409 Impact factor: 6.600