Lessons from SARS: control of acute lung failure by the SARS receptor ACE2

J Mol Med (Berl). 2006 Oct;84(10):814-20. doi: 10.1007/s00109-006-0094-9. Epub 2006 Sep 19.

Abstract

Angiotensin-converting enzyme 2 (ACE2), a second angiotensin-converting enzyme (ACE), regulates the renin-angiotensin system by counterbalancing ACE activity. Accumulating evidence in recent years has demonstrated a physiological and pathological role of ACE2 in the cardiovascular systems. Recently, it has been shown that severe acute respiratory syndrome (SARS) coronavirus, the cause of SARS, utilizes ACE2 as an essential receptor for cell fusion and in vivo infections in mice. Intriguingly, ACE2 acts as a protective factor in various experimental models of acute lung failure and, therefore, acts not only as a key determinant for SARS virus entry into cells but also contributes to SARS pathogenesis. Here we review the role of ACE2 in disease pathogenesis, including lung diseases and cardiovascular diseases.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Angiotensin-Converting Enzyme 2
  • Animals
  • Cardiovascular Diseases / enzymology
  • Cardiovascular Diseases / metabolism
  • Cardiovascular Diseases / therapy
  • Genetic Therapy / methods
  • Humans
  • Lung Diseases / enzymology*
  • Lung Diseases / metabolism
  • Lung Diseases / therapy
  • Mice
  • Models, Biological
  • Peptidyl-Dipeptidase A / genetics
  • Peptidyl-Dipeptidase A / metabolism*
  • SARS Virus / growth & development
  • SARS Virus / metabolism*
  • Severe Acute Respiratory Syndrome / enzymology
  • Severe Acute Respiratory Syndrome / metabolism*
  • Severe Acute Respiratory Syndrome / virology

Substances

  • Peptidyl-Dipeptidase A
  • ACE2 protein, human
  • Ace2 protein, mouse
  • Angiotensin-Converting Enzyme 2