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Angiotensin-converting enzyme 2 protects from severe acute lung failure
Yumiko Imai1, Keiji Kuba, Shuan Rao
1IMBA, Institute of Molecular Biotechnology of the Austrian Academy of Sciences, Vienna A-1030, Austria.
Nature
|July 8, 2005
Summary
Angiotensin-converting enzyme 2 (ACE2) protects against acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Targeting ACE2 may offer a novel therapy for ARDS, a condition with high mortality and limited treatment options.
Area of Science:
- Pulmonary Medicine
- Molecular Biology
- Pathophysiology
Background:
- Acute respiratory distress syndrome (ARDS) is a severe lung injury with high mortality.
- Current treatments for ARDS are limited.
- The renin-angiotensin system (RAS) plays a role in lung injury, with key enzymes ACE and ACE2 having opposing functions.
Purpose of the Study:
- To investigate the role of ACE2 and other RAS components in acute lung injury (ALI).
- To explore the therapeutic potential of targeting ACE2 for ARDS.
- To understand the protective mechanisms of ACE2 in lung injury models.
Main Methods:
- Utilized mouse models of acute lung injury induced by acid aspiration and sepsis.
- Generated mice deficient for Angiotensin-converting enzyme (ACE).
- Administered recombinant ACE2 to assess its protective effects.
Main Results:
- ACE2 and angiotensin II type 2 receptor (AT2) demonstrated protective effects against ALI in mice.
- ACE, angiotensin II, and angiotensin II type 1a receptor (AT1a) were found to promote lung injury.
- Mice deficient for ACE exhibited improved outcomes in ALI models.
- Recombinant ACE2 administration protected mice from severe ALI.
Conclusions:
- ACE2 plays a critical protective role in mitigating acute lung injury.
- Targeting ACE2 presents a promising therapeutic strategy for ARDS.
- Modulating the renin-angiotensin system, specifically enhancing ACE2 activity, could be beneficial for ARDS patients.
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