COVID-19: ACE2centric Infective Disease?

Area of Science:

• Cardiovascular Research
• Pulmonary Medicine
• Infectious Diseases

Background:

• Coronavirus disease 2019 (COVID-19) is characterized by diffuse pulmonary and endothelial inflammation, and enhanced thrombosis.
• These pathological features resemble adverse reactions induced by angiotensin II and counteracted by angiotensin 1-7 in experimental models.
• Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) downregulates ACE2 receptors, crucial for angiotensin II metabolism.

Purpose of the Study:

• To investigate the role of the angiotensin system imbalance in COVID-19 pathogenesis.
• To explore potential therapeutic strategies targeting the angiotensin system for COVID-19 treatment.

Main Methods:

• The study reviews existing experimental models and clinical observations related to COVID-19 and the renin-angiotensin system.
• It analyzes the mechanism of SARS-CoV-2 entry via ACE2 receptors and its downstream effects.
• The rationale for therapeutic interventions is discussed based on the proposed pathophysiological mechanism.

Main Results:

• Downregulation of ACE2 by SARS-CoV-2 leads to reduced inactivation of angiotensin II and decreased generation of angiotensin 1-7.
• This imbalance promotes inflammation and thrombosis, contributing to the clinical manifestations of COVID-19.
• Experimental models of lung injury show similar outcomes due to angiotensin system dysregulation.

Conclusions:

• The imbalance between angiotensin II overactivity and angiotensin 1-7 deficiency is a key factor in COVID-19 pathology.
• Therapeutic approaches such as recombinant ACE2, exogenous angiotensin 1-7, and angiotensin receptor blockers show promise for treating COVID-19.
• Further clinical testing of these strategies is warranted to validate their efficacy.