Key result
COVID-19 may trigger widespread microcirculatory damage by down-regulating ACE2 and deregulating RAAS.
Why the study?
SARS-CoV-2 causes multiform manifestations and multiorgan damage, prompting a review of available data to explore COVID-19 as a transient molecular disease causing ACE2 down-regulation, RAAS dysregulation, and microcirculatory changes.
This review proposes a unifying pathophysiological model of COVID-19 driven by ACE2 down-regulation and RAAS dysregulation causing microcirculatory damage.
Hypothesis-generating for RAAS-targeted therapies in COVID-19 vasculopathy; leaves open need for prospective trials before clinical adoption.
Severe acute respiratory syndrome coronavirus 2, the etiologic agent of coronavirus disease 2019 (COVID-19) 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 assessment of the data already available for COVID-19, exploring it as a transient molecular disease that causes negative regulation of angiotensin-converting enzyme 2, and consequently, deregulates the renin-angiotensin-aldosterone system, promoting important changes in the microcirculatory environment. Another goal of the article is to show how these microcirculatory changes may be responsible for the wide variety of injury mechanisms observed in different organs in this disease. The new concept of COVID-19 provides a unifying pathophysiological picture of this infection and offers fresh insights for a rational treatment strategy to combat this ongoing pandemic.
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Ramos et al. (2021) conducted a review in COVID-19. ACE2 down-regulation was evaluated. COVID-19 may act as a transient molecular disease that down-regulates ACE2 and deregulates the renin-angiotensin-aldosterone system, leading to widespread microcirculatory tissue damage.
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