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.

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 / S.G. Ramos, B.A.D.C. Rattis, G. Ottaviani, M.R.N. Celes, E.P. Dias. - In: THE AMERICAN JOURNAL OF PATHOLOGY. - ISSN 0002-9440. - 191:7(2021 Jul), pp. 1154-1164. [10.1016/j.ajpath.2021.04.010]

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

G. Ottaviani
Conceptualization
;
2021-07

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.
ACE-2; Ang II; COVID-19; Immunothrombosis; Microcirculation; Molecular disease; Pathogenesis; Thromboinflammation
Settore MED/08 - Anatomia Patologica
giu-2021
https://pubmed.ncbi.nlm.nih.gov/33964216/
Centro di Ricerca "Lino Rossi" per lo studio e la prevenzione della morte perinatale del feto a termine e neonatale e della sindrome della morte improvvisa del lattante SIDS
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/2434/845255
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