SrasV1, PubMed, Curation, bibRecord, 002654

Angiotensin-converting enzyme 2 protects from severe acute lung failure.

Identifieur interne : 002654 ( PubMed/Curation ); précédent : 002653; suivant : 002655

Angiotensin-converting enzyme 2 protects from severe acute lung failure.

Auteurs : Yumiko Imai [Autriche] ; 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 ; Josef M. Penninger

Source :

Nature [ 1476-4687 ] ; 2005.

RBID : pubmed:16001071

Descripteurs français

KwdFr :
- Acides (pharmacologie), Analyse de variance, Angiotensine-II (métabolisme), Animaux, Carboxypeptidases (déficit), Carboxypeptidases (génétique), Carboxypeptidases (métabolisme), Délétion de gène, Humains, Maladie aigüe, Maladies pulmonaires (anatomopathologie), Maladies pulmonaires (enzymologie), Maladies pulmonaires (génétique), Maladies pulmonaires (physiopathologie), Modèles animaux de maladie humaine, Oedème pulmonaire (anatomopathologie), Oedème pulmonaire (physiopathologie), Oxygène (sang), Peptidyl-Dipeptidase A, Perméabilité capillaire, Poumon (anatomopathologie), Poumon (physiopathologie), Récepteur de type 1 à l'angiotensine-II (métabolisme), Récepteur de type 2 à l'angiotensine-II (métabolisme), Sepsie (anatomopathologie), Sepsie (enzymologie), Sepsie (génétique), Souris, Souris knockout, Souris transgéniques, Syndrome de détresse respiratoire de l'adulte (anatomopathologie), Syndrome de détresse respiratoire de l'adulte (enzymologie), Syndrome de détresse respiratoire de l'adulte (génétique), Transgènes (génétique).
MESH :
- anatomopathologie : Maladies pulmonaires, Oedème pulmonaire, Poumon, Sepsie, Syndrome de détresse respiratoire de l'adulte.
- déficit : Carboxypeptidases.
- enzymologie : Maladies pulmonaires, Sepsie, Syndrome de détresse respiratoire de l'adulte.
- génétique : Carboxypeptidases, Maladies pulmonaires, Sepsie, Syndrome de détresse respiratoire de l'adulte, Transgènes.
- métabolisme : Angiotensine-II, Carboxypeptidases, Récepteur de type 1 à l'angiotensine-II, Récepteur de type 2 à l'angiotensine-II.
- pharmacologie : Acides.
- physiopathologie : Maladies pulmonaires, Oedème pulmonaire, Poumon.
- sang : Oxygène.
- Analyse de variance, Animaux, Délétion de gène, Humains, Maladie aigüe, Modèles animaux de maladie humaine, Peptidyl-Dipeptidase A, Perméabilité capillaire, Souris, Souris knockout, Souris transgéniques.

English descriptors

KwdEn :
- Acids (pharmacology), Acute Disease, Analysis of Variance, Angiotensin II (metabolism), Animals, Capillary Permeability, Carboxypeptidases (deficiency), Carboxypeptidases (genetics), Carboxypeptidases (metabolism), Disease Models, Animal, Gene Deletion, Humans, Lung (pathology), Lung (physiopathology), Lung Diseases (enzymology), Lung Diseases (genetics), Lung Diseases (pathology), Lung Diseases (physiopathology), Mice, Mice, Knockout, Mice, Transgenic, Oxygen (blood), Peptidyl-Dipeptidase A, Pulmonary Edema (pathology), Pulmonary Edema (physiopathology), Receptor, Angiotensin, Type 1 (metabolism), Receptor, Angiotensin, Type 2 (metabolism), Respiratory Distress Syndrome, Adult (enzymology), Respiratory Distress Syndrome, Adult (genetics), Respiratory Distress Syndrome, Adult (pathology), Sepsis (enzymology), Sepsis (genetics), Sepsis (pathology), Transgenes (genetics).
MESH :
- chemical , blood : Oxygen.
- chemical , deficiency : Carboxypeptidases.
- chemical , genetics : Carboxypeptidases.
- chemical , metabolism : Angiotensin II, Carboxypeptidases, Receptor, Angiotensin, Type 1, Receptor, Angiotensin, Type 2.
- chemical , pharmacology : Acids.
- enzymology : Lung Diseases, Respiratory Distress Syndrome, Adult, Sepsis.
- genetics : Lung Diseases, Respiratory Distress Syndrome, Adult, Sepsis, Transgenes.
- pathology : Lung, Lung Diseases, Pulmonary Edema, Respiratory Distress Syndrome, Adult, Sepsis.
- physiopathology : Lung, Lung Diseases, Pulmonary Edema.
- Acute Disease, Analysis of Variance, Animals, Capillary Permeability, Disease Models, Animal, Gene Deletion, Humans, Mice, Mice, Knockout, Mice, Transgenic, Peptidyl-Dipeptidase A.

Abstract

Acute respiratory distress syndrome (ARDS), the most severe form of acute lung injury, is a devastating clinical syndrome with a high mortality rate (30-60%) (refs 1-3). Predisposing factors for ARDS are diverse and include sepsis, aspiration, pneumonias and infections with the severe acute respiratory syndrome (SARS) coronavirus. At present, there are no effective drugs for improving the clinical outcome of ARDS. Angiotensin-converting enzyme (ACE) and ACE2 are homologues with different key functions in the renin-angiotensin system. ACE cleaves angiotensin I to generate angiotensin II, whereas ACE2 inactivates angiotensin II and is a negative regulator of the system. ACE2 has also recently been identified as a potential SARS virus receptor and is expressed in lungs. Here we report that ACE2 and the angiotensin II type 2 receptor (AT2) protect mice from severe acute lung injury induced by acid aspiration or sepsis. However, other components of the renin-angiotensin system, including ACE, angiotensin II and the angiotensin II type 1a receptor (AT1a), promote disease pathogenesis, induce lung oedemas and impair lung function. We show that mice deficient for Ace show markedly improved disease, and also that recombinant ACE2 can protect mice from severe acute lung injury. Our data identify a critical function for ACE2 in acute lung injury, pointing to a possible therapy for a syndrome affecting millions of people worldwide every year.

DOI: 10.1038/nature03712
PubMed: 16001071

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<term>Animals</term>
<term>Capillary Permeability</term>
<term>Carboxypeptidases (deficiency)</term>
<term>Carboxypeptidases (genetics)</term>
<term>Carboxypeptidases (metabolism)</term>
<term>Disease Models, Animal</term>
<term>Gene Deletion</term>
<term>Humans</term>
<term>Lung (pathology)</term>
<term>Lung (physiopathology)</term>
<term>Lung Diseases (enzymology)</term>
<term>Lung Diseases (genetics)</term>
<term>Lung Diseases (pathology)</term>
<term>Lung Diseases (physiopathology)</term>
<term>Mice</term>
<term>Mice, Knockout</term>
<term>Mice, Transgenic</term>
<term>Oxygen (blood)</term>
<term>Peptidyl-Dipeptidase A</term>
<term>Pulmonary Edema (pathology)</term>
<term>Pulmonary Edema (physiopathology)</term>
<term>Receptor, Angiotensin, Type 1 (metabolism)</term>
<term>Receptor, Angiotensin, Type 2 (metabolism)</term>
<term>Respiratory Distress Syndrome, Adult (enzymology)</term>
<term>Respiratory Distress Syndrome, Adult (genetics)</term>
<term>Respiratory Distress Syndrome, Adult (pathology)</term>
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<term>Analyse de variance</term>
<term>Angiotensine-II (métabolisme)</term>
<term>Animaux</term>
<term>Carboxypeptidases (déficit)</term>
<term>Carboxypeptidases (génétique)</term>
<term>Carboxypeptidases (métabolisme)</term>
<term>Délétion de gène</term>
<term>Humains</term>
<term>Maladie aigüe</term>
<term>Maladies pulmonaires (anatomopathologie)</term>
<term>Maladies pulmonaires (enzymologie)</term>
<term>Maladies pulmonaires (génétique)</term>
<term>Maladies pulmonaires (physiopathologie)</term>
<term>Modèles animaux de maladie humaine</term>
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<term>Oedème pulmonaire (physiopathologie)</term>
<term>Oxygène (sang)</term>
<term>Peptidyl-Dipeptidase A</term>
<term>Perméabilité capillaire</term>
<term>Poumon (anatomopathologie)</term>
<term>Poumon (physiopathologie)</term>
<term>Récepteur de type 1 à l'angiotensine-II (métabolisme)</term>
<term>Récepteur de type 2 à l'angiotensine-II (métabolisme)</term>
<term>Sepsie (anatomopathologie)</term>
<term>Sepsie (enzymologie)</term>
<term>Sepsie (génétique)</term>
<term>Souris</term>
<term>Souris knockout</term>
<term>Souris transgéniques</term>
<term>Syndrome de détresse respiratoire de l'adulte (anatomopathologie)</term>
<term>Syndrome de détresse respiratoire de l'adulte (enzymologie)</term>
<term>Syndrome de détresse respiratoire de l'adulte (génétique)</term>
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<term>Receptor, Angiotensin, Type 2</term>
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<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Maladies pulmonaires</term>
<term>Oedème pulmonaire</term>
<term>Poumon</term>
<term>Sepsie</term>
<term>Syndrome de détresse respiratoire de l'adulte</term>
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<term>Respiratory Distress Syndrome, Adult</term>
<term>Sepsis</term>
<term>Transgenes</term>
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<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Carboxypeptidases</term>
<term>Maladies pulmonaires</term>
<term>Sepsie</term>
<term>Syndrome de détresse respiratoire de l'adulte</term>
<term>Transgènes</term>
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<term>Récepteur de type 2 à l'angiotensine-II</term>
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<term>Lung Diseases</term>
<term>Pulmonary Edema</term>
<term>Respiratory Distress Syndrome, Adult</term>
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<term>Analysis of Variance</term>
<term>Animals</term>
<term>Capillary Permeability</term>
<term>Disease Models, Animal</term>
<term>Gene Deletion</term>
<term>Humans</term>
<term>Mice</term>
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<term>Mice, Transgenic</term>
<term>Peptidyl-Dipeptidase A</term>
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<term>Humains</term>
<term>Maladie aigüe</term>
<term>Modèles animaux de maladie humaine</term>
<term>Peptidyl-Dipeptidase A</term>
<term>Perméabilité capillaire</term>
<term>Souris</term>
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<front><div type="abstract" xml:lang="en">Acute respiratory distress syndrome (ARDS), the most severe form of acute lung injury, is a devastating clinical syndrome with a high mortality rate (30-60%) (refs 1-3). Predisposing factors for ARDS are diverse and include sepsis, aspiration, pneumonias and infections with the severe acute respiratory syndrome (SARS) coronavirus. At present, there are no effective drugs for improving the clinical outcome of ARDS. Angiotensin-converting enzyme (ACE) and ACE2 are homologues with different key functions in the renin-angiotensin system. ACE cleaves angiotensin I to generate angiotensin II, whereas ACE2 inactivates angiotensin II and is a negative regulator of the system. ACE2 has also recently been identified as a potential SARS virus receptor and is expressed in lungs. Here we report that ACE2 and the angiotensin II type 2 receptor (AT2) protect mice from severe acute lung injury induced by acid aspiration or sepsis. However, other components of the renin-angiotensin system, including ACE, angiotensin II and the angiotensin II type 1a receptor (AT1a), promote disease pathogenesis, induce lung oedemas and impair lung function. We show that mice deficient for Ace show markedly improved disease, and also that recombinant ACE2 can protect mice from severe acute lung injury. Our data identify a critical function for ACE2 in acute lung injury, pointing to a possible therapy for a syndrome affecting millions of people worldwide every year.</div>
</front>
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<Month>07</Month>
<Day>19</Day>
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<ArticleTitle>Angiotensin-converting enzyme 2 protects from severe acute lung failure.</ArticleTitle>
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<Abstract><AbstractText>Acute respiratory distress syndrome (ARDS), the most severe form of acute lung injury, is a devastating clinical syndrome with a high mortality rate (30-60%) (refs 1-3). Predisposing factors for ARDS are diverse and include sepsis, aspiration, pneumonias and infections with the severe acute respiratory syndrome (SARS) coronavirus. At present, there are no effective drugs for improving the clinical outcome of ARDS. Angiotensin-converting enzyme (ACE) and ACE2 are homologues with different key functions in the renin-angiotensin system. ACE cleaves angiotensin I to generate angiotensin II, whereas ACE2 inactivates angiotensin II and is a negative regulator of the system. ACE2 has also recently been identified as a potential SARS virus receptor and is expressed in lungs. Here we report that ACE2 and the angiotensin II type 2 receptor (AT2) protect mice from severe acute lung injury induced by acid aspiration or sepsis. However, other components of the renin-angiotensin system, including ACE, angiotensin II and the angiotensin II type 1a receptor (AT1a), promote disease pathogenesis, induce lung oedemas and impair lung function. We show that mice deficient for Ace show markedly improved disease, and also that recombinant ACE2 can protect mice from severe acute lung injury. Our data identify a critical function for ACE2 in acute lung injury, pointing to a possible therapy for a syndrome affecting millions of people worldwide every year.</AbstractText>
</Abstract>
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<ArticleIdList><ArticleId IdType="pubmed">16001071</ArticleId>
<ArticleId IdType="pii">nature03712</ArticleId>
<ArticleId IdType="doi">10.1038/nature03712</ArticleId>
<ArticleId IdType="pmc">PMC7094998</ArticleId>
</ArticleIdList>
<ReferenceList><Reference><Citation>N Engl J Med. 2003 May 15;348(20):1977-85</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12671062</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>JAMA. 2003 Apr 23-30;289(16):2104-12</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12709468</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>Nature. 2003 Nov 27;426(6965):450-4</Citation>
<ArticleIdList><ArticleId IdType="pubmed">14647384</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>Am J Respir Crit Care Med. 1995 Feb;151(2 Pt 1):293-301</Citation>
<ArticleIdList><ArticleId IdType="pubmed">7842182</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>J Pathol. 2004 Jun;203(2):631-7</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15141377</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>Circ Res. 2000 Sep 1;87(5):E1-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">10969042</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>Hypertension. 1994 Nov;24(5):531-7</Citation>
<ArticleIdList><ArticleId IdType="pubmed">7960011</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>Nat Med. 2004 Feb;10(2):155-60</Citation>
<ArticleIdList><ArticleId IdType="pubmed">14704790</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>Nat Immunol. 2000 Jul;1(1):42-6</Citation>
<ArticleIdList><ArticleId IdType="pubmed">10881173</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>N Engl J Med. 2003 May 15;348(20):1953-66</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12690092</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>Am J Physiol. 1996 Jul;271(1 Pt 2):H222-7</Citation>
<ArticleIdList><ArticleId IdType="pubmed">8760178</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>J Appl Physiol (1985). 1985 Mar;58(3):812-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">3980386</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>J Biol Chem. 1995 Aug 11;270(32):18719-22</Citation>
<ArticleIdList><ArticleId IdType="pubmed">7642517</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>Can J Physiol Pharmacol. 1996 Jul;74(7):824-33</Citation>
<ArticleIdList><ArticleId IdType="pubmed">8946069</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>Methods Enzymol. 1995;248:283-305</Citation>
<ArticleIdList><ArticleId IdType="pubmed">7674927</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>N Engl J Med. 2000 May 4;342(18):1334-49</Citation>
<ArticleIdList><ArticleId IdType="pubmed">10793167</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>N Engl J Med. 2003 May 15;348(20):1986-94</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12682352</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>Adv Exp Med Biol. 1980;130:1-27</Citation>
<ArticleIdList><ArticleId IdType="pubmed">6250339</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>N Engl J Med. 2003 May 15;348(20):1967-76</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12690091</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>Am J Respir Crit Care Med. 2002 Sep 1;166(5):646-50</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12204859</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>Nature. 2002 Jun 20;417(6891):822-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12075344</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>Nature. 1995 May 11;375(6527):146-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">7753170</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>N Engl J Med. 2003 May 15;348(20):1995-2005</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12671061</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>N Engl J Med. 2004 Mar 18;350(12):1179-88</Citation>
<ArticleIdList><ArticleId IdType="pubmed">14985470</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>Nature. 1995 Oct 26;377(6551):744-7</Citation>
<ArticleIdList><ArticleId IdType="pubmed">7477266</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>Adv Exp Med Biol. 1995;377:311-7</Citation>
<ArticleIdList><ArticleId IdType="pubmed">7484433</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>N Engl J Med. 2002 Nov 28;347(22):1795-7</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12456857</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>Am J Physiol Lung Cell Mol Physiol. 2003 Dec;285(6):L1222-32</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12909586</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>J Biol Chem. 2000 Oct 27;275(43):33238-43</Citation>
<ArticleIdList><ArticleId IdType="pubmed">10924499</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList><Reference><Citation>Crit Care Med. 2003 Apr;31(4 Suppl):S296-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12682455</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
</PubmedData>
</pubmed>
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Angiotensin-converting enzyme 2 protects from severe acute lung failure.

Angiotensin-converting enzyme 2 protects from severe acute lung failure.

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