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Angiotensin-converting enzyme 2 protects from severe acute lung failure

Author

Listed:
  • 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)

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.

Suggested Citation

  • 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 & S, 2005. "Angiotensin-converting enzyme 2 protects from severe acute lung failure," Nature, Nature, vol. 436(7047), pages 112-116, July.
    • Handle: RePEc:nat:nature:v:436:y:2005:i:7047:d:10.1038_nature03712
    DOI: 10.1038/nature03712
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    Cited by:

    1. Tomokazu Yamaguchi & Midori Hoshizaki & Takafumi Minato & Satoru Nirasawa & Masamitsu N. Asaka & Mayumi Niiyama & Masaki Imai & Akihiko Uda & Jasper Fuk-Woo Chan & Saori Takahashi & Jianbo An & Akari , 2021. "ACE2-like carboxypeptidase B38-CAP protects from SARS-CoV-2-induced lung injury," Nature Communications, Nature, vol. 12(1), pages 1-13, December.
    2. Milad Haghani & Pegah Varamini, 2021. "Temporal evolution, most influential studies and sleeping beauties of the coronavirus literature," Scientometrics, Springer;Akadémiai Kiadó, vol. 126(8), pages 7005-7050, August.
    3. Jung-Hyun Kim & Jeeyoung Kim & Woo Jin Kim & Yung Hyun Choi & Se-Ran Yang & Seok-Ho Hong, 2020. "Diesel Particulate Matter 2.5 Induces Epithelial-to-Mesenchymal Transition and Upregulation of SARS-CoV-2 Receptor during Human Pluripotent Stem Cell-Derived Alveolar Organoid Development," IJERPH, MDPI, vol. 17(22), pages 1-15, November.
    4. Steven Andrew Baker & Shirley Kwok & Gerald J Berry & Thomas J Montine, 2021. "Angiotensin-converting enzyme 2 (ACE2) expression increases with age in patients requiring mechanical ventilation," PLOS ONE, Public Library of Science, vol. 16(2), pages 1-17, February.

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