SARS-CoV-2 Pathogenesis: Imbalance in the Renin-Angiotensin System Favors Lung Fibrosis

Front Cell Infect Microbiol. 2020 Jun 12:10:340. doi: 10.3389/fcimb.2020.00340. eCollection 2020.
No abstract available

Keywords: ACE2; ANG1-7; Fibrosis; Renin angiotensin system (RAS); SARS-CoV-2.

MeSH terms

  • Alveolar Epithelial Cells / enzymology
  • Angiotensin I / metabolism
  • Angiotensin I / pharmacology
  • Angiotensin II / metabolism
  • Angiotensin-Converting Enzyme 2
  • Betacoronavirus / pathogenicity*
  • Betacoronavirus / physiology
  • COVID-19
  • Coronavirus Infections / complications*
  • Coronavirus Infections / physiopathology
  • Coronavirus Infections / virology*
  • Host Microbial Interactions
  • Humans
  • Lung / enzymology
  • Lung / physiopathology
  • Lung / virology
  • Pandemics
  • Peptide Fragments / metabolism
  • Peptide Fragments / pharmacology
  • Peptidyl-Dipeptidase A / genetics
  • Peptidyl-Dipeptidase A / metabolism*
  • Pneumonia, Viral / complications*
  • Pneumonia, Viral / physiopathology
  • Pneumonia, Viral / virology*
  • Pulmonary Fibrosis / etiology*
  • Receptors, Coronavirus
  • Receptors, Virus / genetics
  • Receptors, Virus / metabolism
  • Renin-Angiotensin System / physiology*
  • SARS-CoV-2
  • Transforming Growth Factor beta / antagonists & inhibitors
  • Transforming Growth Factor beta / metabolism

Substances

  • Peptide Fragments
  • Receptors, Coronavirus
  • Receptors, Virus
  • Transforming Growth Factor beta
  • Angiotensin II
  • Angiotensin I
  • Peptidyl-Dipeptidase A
  • ACE2 protein, human
  • Angiotensin-Converting Enzyme 2
  • angiotensin I (1-7)