tetano
Editor, Senior Moderator
Am J Pathol
. 2021 May 5;S0002-9440(21)00194-2.
doi: 10.1016/j.ajpath.2021.04.010. Online ahead of print.
ACE-2 down-regulation may act as a transient molecular disease causing RAAS dysregulation and tissue damage in the microcirculatory environment among COVID-19 patients
Simone Gusm?o Ramos[SUP] 1 [/SUP], Bruna Amanda da Cruz Rattis[SUP] 2 [/SUP], Giulia Ottaviani[SUP] 3 [/SUP], Mara Rubia Nunes Celes[SUP] 4 [/SUP], Eliane Pedra Dias[SUP] 5 [/SUP]
Affiliations
Abstract
SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2), the etiological agent of COVID-19 (coronavirus disease 2019) and the cause of the current pandemic, produces multiform manifestations throughout the body, causing indiscriminate damage to multiple organ systems, particularly the lungs, heart, brain, kidney, and vasculature. The aim of this review is to provide a new look at the data already available for COVID-19, exploring it as a transient molecular disease that causes negative regulation of ACE-2 (angiotensin-converting enzyme 2) and, consequently, deregulates the renin-angiotensin-aldosterone system (RAAS), promoting important changes in the microcirculatory environment. In addition, the authors seek to demonstrate how these microcirculatory changes may be responsible for the wide variety of injury mechanisms observed in different organs in this disease. This new proposed concept of COVID-19 provides a unifying pathophysiological picture of this infection and offers new insights for a rational treatment strategy to combat this new pandemic.
Keywords: ACE-2; Ang II; COVID-19; Immunothrombosis; Microcirculation; Molecular disease; Pathogenesis; Thromboinflammation.
. 2021 May 5;S0002-9440(21)00194-2.
doi: 10.1016/j.ajpath.2021.04.010. Online ahead of print.
ACE-2 down-regulation may act as a transient molecular disease causing RAAS dysregulation and tissue damage in the microcirculatory environment among COVID-19 patients
Simone Gusm?o Ramos[SUP] 1 [/SUP], Bruna Amanda da Cruz Rattis[SUP] 2 [/SUP], Giulia Ottaviani[SUP] 3 [/SUP], Mara Rubia Nunes Celes[SUP] 4 [/SUP], Eliane Pedra Dias[SUP] 5 [/SUP]
Affiliations
- PMID: 33964216
- DOI: 10.1016/j.ajpath.2021.04.010
Abstract
SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2), the etiological agent of COVID-19 (coronavirus disease 2019) and the cause of the current pandemic, produces multiform manifestations throughout the body, causing indiscriminate damage to multiple organ systems, particularly the lungs, heart, brain, kidney, and vasculature. The aim of this review is to provide a new look at the data already available for COVID-19, exploring it as a transient molecular disease that causes negative regulation of ACE-2 (angiotensin-converting enzyme 2) and, consequently, deregulates the renin-angiotensin-aldosterone system (RAAS), promoting important changes in the microcirculatory environment. In addition, the authors seek to demonstrate how these microcirculatory changes may be responsible for the wide variety of injury mechanisms observed in different organs in this disease. This new proposed concept of COVID-19 provides a unifying pathophysiological picture of this infection and offers new insights for a rational treatment strategy to combat this new pandemic.
Keywords: ACE-2; Ang II; COVID-19; Immunothrombosis; Microcirculation; Molecular disease; Pathogenesis; Thromboinflammation.