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 path-ogenesis of COVID19 is still a matter of debate. RAAS represents an important protagonist in the pathogenesis of COVID19, providing the virus with the receptor of entry into host cells and deter-mining 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 con-tribute to the establishment of the thrombo-inflammatory state characteristic of severe forms of COVID19. Drugs targeting RAAS represent promising therapeutic options for COVID19 sufferers. © 2021 by the authors. Licensee MDPI, Basel, Switzerland.
Lock, Stock and Barrel: Role of Renin-Angiotensin-Aldosterone System in Coronavirus Disease 2019
Franceschi, Francesco;Ojetti, Veronica;
2021-01-01
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 path-ogenesis of COVID19 is still a matter of debate. RAAS represents an important protagonist in the pathogenesis of COVID19, providing the virus with the receptor of entry into host cells and deter-mining 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 con-tribute to the establishment of the thrombo-inflammatory state characteristic of severe forms of COVID19. Drugs targeting RAAS represent promising therapeutic options for COVID19 sufferers. © 2021 by the authors. Licensee MDPI, Basel, Switzerland.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
