[Inhibitors of RAS Might Be a Good Choice for the Therapy of COVID-19 Pneumonia]

M L Sun1, J M Yang2, Y P Sun1

  • 1Department of Oncology, Jinan Central Hospital Affiliated to Shandong University, Jinan 250013, China.

Insights

This study explores how COVID-19 disrupts the renin-angiotensin system (RAS) by targeting ACE2, potentially worsening pneumonia. Researchers suggest RAS inhibitors may reduce inflammation and mortality in COVID-19 patients.

Area of Science:

  • Cardiovascular Research
  • Infectious Diseases
  • Pulmonary Medicine

Background:

  • COVID-19 infection involves binding to human ACE2, causing severe pneumonia and high mortality.
  • The renin-angiotensin system (RAS) plays a critical role in regulating inflammation and cardiovascular function.
  • Imbalance in RAS pathways, specifically the ACE/Ang II/AT1R and ACE2/Ang (1-7)/Mas receptor axes, is linked to multi-system inflammation.

Purpose of the Study:

  • To investigate the role of RAS dysregulation in COVID-19 pathogenesis.
  • To explore the potential therapeutic benefits of RAS inhibitors in managing COVID-19 pneumonia.

Main Methods:

  • Review of existing literature on COVID-19, ACE2 function, and the RAS.
  • Analysis of the impact of SARS-CoV-2 binding to ACE2 on RAS pathway activity.
  • Extrapolation of findings from animal studies on RAS inhibitors in acute lung injury.

Main Results:

  • COVID-19 binding to ACE2 leads to ACE2 exhaustion and inhibition of the ACE2/Ang (1-7)/Mas receptor pathway.
  • This disruption of the RAS balance exacerbates acute severe pneumonia.
  • Elevated ACE and Angiotensin II are identified as negative prognostic factors in severe pneumonia.

Conclusions:

  • ACE2 depletion by SARS-CoV-2 disrupts the RAS, contributing to severe COVID-19 outcomes.
  • ACE inhibitors (ACEI) and AT1 receptor (AT1R) inhibitors are hypothesized to mitigate pulmonary inflammation and reduce mortality in COVID-19 patients, provided blood pressure is controlled.

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