ACE2 Down-Regulation May Act as a Transient Molecular Disease Causing RAAS Dysregulation and Tissue Damage in the Microcirculatory Environment Among COVID-19 Patients

Autor(es)

Ramos, Simone Gusmao ^[1] ; da Cruz Rattis, Bruna Amanda ^[1] ; Ottaviani, Giulia ^[2] ; Nunes Celes, Mara Rubia ^{[3, 1]} ; Dias, Eliane Pedra ^[4]

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Dept Pathol & Forens Med, Ribeirao Preto Med Sch, BR-14049900 Ribeirao Preto, SP - Brazil

^[2] Univ Milan, Ctr Ric Lino Rossi, Anat Pathol MED 08, Milan - Italy

^[3] Univ Fed Goias, Inst Trop Pathol & Publ Hlth, Dept Biosci & Technol, Goiania, Go - Brazil

^[4] Fluminense Fed Univ, Fac Med, Dept Pathol, Niteroi, RJ - Brazil

• Tipo de documento: Artigo de Revisão
• Fonte: American Journal of Pathology; v. 191, n. 7, p. 1154-1164, JUL 2021.
• Citações Web of Science: 0

Resumo

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. (AU)

• Processo FAPESP: 12/23649-0 - Cardiomiopatia séptica como componente da síndrome de falência de múltiplos órgãos na sépsis grave
• Beneficiário: Simone Gusmão Ramos
• Modalidade de apoio: Auxílio à Pesquisa - Regular