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This Article Full Text Full Text (PDF) All Versions of this Article: 93/5/543    most recent expphysiol.2007.040048v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Google Scholar Articles by Imai, Y. Articles by Penninger, J. M. PubMed PubMed Citation Articles by Imai, Y. Articles by Penninger, J. M. Related Collections Respiratory Review Articles

¹ The Global Center of Excellence program, Akita University Graduate School of Medicine, Akita 010-8543, Japan ² Medical Top Track Program, Medical Research Institute, Tokyo Medical and Dental University, Tokyo 101-0062, Japan ³ Institute of Molecular Biotechnology of the Austrian Academy of Sciences, Dr. Bohr-gasse 3, Vienna, A-1030, Austria

During several months of 2002, severe acute respiratory syndrome (SARS) caused by SARS-coronavirus (SARS-CoV) spread rapidly from China throughout the world, causing more than 800 deaths due to the development of acute respiratory distress syndrome (ARDS), which is the severe form of acute lung injury (ALI). Interestingly, a novel homologue of angiotensin-converting enzyme, termed angiotensin-converting enzyme 2 (ACE2), has been identified as a receptor for SARS-CoV. Angiotensin-converting enzyme and ACE2 share homology in their catalytic domain and provide different key functions in the renin–angiotensin system (RAS). Angiotensin-converting enzyme cleaves angiotensin I to generate angiotensin II, which is a key effector peptide of the system and exerts multiple biological functions, whereas ACE2 reduces angiotensin II levels. Importantly, our recent studies using ACE2 knockout mice have demonstrated that ACE2 protects murine lungs from ARDS. Furthermore, SARS-CoV infections and the Spike protein of the SARS-CoV reduce ACE2 expression. Notably, injection of SARS-CoV Spike into mice worsens acute lung failure in vivo, which can be attenuated by blocking the renin–angiotensin pathway, suggesting that the activation of the pulmonary RAS influences the pathogenesis of ALI/ARDS and SARS.

(Received 5 March 2008; accepted after revision 13 March 2008; first published online 10 April 2008)
Corresponding author J. M. Penninger: Institute of Molecular Biotechnology of the Austrian Academy of Sciences, Dr. Bohr-gasse 3, Vienna, A-1030, Austria.  Email: josef.penninger{at}imba.oeaw.ac.at

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