Angiotensin-converting enzyme 2 protects from severe acute lung failure

Yumiko Imai, Keiji Kuba, Shuan Rao, Yi Huan, Feng Guo, Bin Guan, Peng Yang, Renu Sarao, Teiji Wada, Howard Leong-Poi, Michael A. Crackower, Akiyoshi Fukamizu, Chi-Chung Hui, Lutz Hein, Stefan Uhlig, Arthur S. Slutsky, Chengyu Jiang and Josef M. Penninger ()
Additional contact information
Yumiko Imai: IMBA, Institute of Molecular Biotechnology of the Austrian Academy of Sciences
Keiji Kuba: IMBA, Institute of Molecular Biotechnology of the Austrian Academy of Sciences
Shuan Rao: Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College
Yi Huan: Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College
Feng Guo: Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College
Bin Guan: Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College
Peng Yang: Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College
Renu Sarao: IMBA, Institute of Molecular Biotechnology of the Austrian Academy of Sciences
Teiji Wada: IMBA, Institute of Molecular Biotechnology of the Austrian Academy of Sciences
Howard Leong-Poi: St. Michael's Hospital
Michael A. Crackower: Merck Frosst Centre for Therapeutic Research
Akiyoshi Fukamizu: University of Tsukuba
Chi-Chung Hui: University of Toronto
Lutz Hein: University of Freiburg
Stefan Uhlig: Research Center Borstel
Arthur S. Slutsky: University of Toronto, St. Michael's Hospital
Chengyu Jiang: Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College
Josef M. Penninger: IMBA, Institute of Molecular Biotechnology of the Austrian Academy of Sciences

Nature, 2005, vol. 436, issue 7047, 112-116

Abstract: Drug hope for SARS The SARS (severe acute respiratory syndrome) epidemic of 2003 caused almost 800 deaths, many of them due to acute respiratory distress syndrome (ARDS) as a complication. There are no effective drugs available for treating ARDS, but new work in mice suggests that ACE2 (angiotensin-converting enzyme 2) might be an option. ACE2 can protect mice from lung injury in an ARDS-like syndrome, whereas other components of the renin–angiotensin system for controlling blood pressure and salt balance actually make the condition worse. ACE2 is expressed in the healthy lung but downregulated by lung injury and it was shown recently (Nature 426, 450–454; 2003) to be a receptor for the SARS coronavirus.

Date: 2005
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DOI: 10.1038/nature03712

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