Endothelial dysfunction and COVID-19 (Review).

Area of Science:

• Cardiovascular Medicine
• Infectious Diseases
• Pharmacology

Background:

• Comorbidities like hypertension significantly increase COVID-19 severity and mortality.
• Hypertension and the renin-angiotensin-aldosterone system (RAAS) contribute to vascular inflammation and endothelial dysfunction (ED), key factors in COVID-19 pathogenesis.
• Angiotensin-converting enzyme 2 (ACE2) is the cellular receptor for SARS-CoV-2 and a critical component of the RAAS.

Purpose of the Study:

• To investigate the role of RAAS, specifically ACE2, in COVID-19 severity.
• To explore the potential therapeutic benefits of targeting ACE2 and related pathways in managing COVID-19.
• To understand how targeting ED can alleviate COVID-19 symptoms and reduce fatalities.

Main Methods:

• Review of existing literature on hypertension, RAAS, ACE2, and COVID-19.
• Analysis of the mechanistic links between RAAS inhibition, ACE2 expression, and SARS-CoV-2 infection.
• Examination of the role of endothelial dysfunction and hypercoagulation in COVID-19 pathogenesis.

Main Results:

• RAAS inhibitors (ACE inhibitors, ARBs) may enhance ACE2 expression, potentially reducing lung injury.
• Increased ACE2 activity could decrease angiotensin II levels, mitigating inflammation and viral entry.
• COVID-19 is characterized by excessive blood clotting, highlighting the importance of coagulation pathways.

Conclusions:

• Targeting ACE2 presents a promising therapeutic strategy for SARS-CoV-2 infection and associated injuries.
• Modulating the RAAS pathway may help reverse COVID-19-induced hypercoagulation and reduce mortality.
• Further research into recombinant human ACE2 and anti-spike monoclonal antibodies is crucial for clinical application.