The discovery of angiotensin-converting enzyme 2 and its role in acute lung injury in mice.
Identifieur interne : 002F92 ( Main/Exploration ); précédent : 002F91; suivant : 002F93The discovery of angiotensin-converting enzyme 2 and its role in acute lung injury in mice.
Auteurs : Yumiko Imai [Japon] ; Keiji Kuba ; Josef M. PenningerSource :
- Experimental physiology [ 0958-0670 ] ; 2008.
Descripteurs français
- KwdFr :
- Animaux, Maladie aigüe, Maladies pulmonaires (anatomopathologie), Maladies pulmonaires (enzymologie), Oedème pulmonaire (anatomopathologie), Oedème pulmonaire (génétique), Peptidyl-Dipeptidase A (physiologie), Souris, Syndrome de détresse respiratoire de l'adulte (anatomopathologie), Syndrome de détresse respiratoire de l'adulte (génétique), Syndrome respiratoire aigu sévère (anatomopathologie), Syndrome respiratoire aigu sévère (génétique), Virus du SRAS (pathogénicité).
- MESH :
- anatomopathologie : Maladies pulmonaires, Oedème pulmonaire, Syndrome de détresse respiratoire de l'adulte, Syndrome respiratoire aigu sévère.
- enzymologie : Maladies pulmonaires.
- génétique : Oedème pulmonaire, Syndrome de détresse respiratoire de l'adulte, Syndrome respiratoire aigu sévère.
- pathogénicité : Virus du SRAS.
- physiologie : Peptidyl-Dipeptidase A.
- Animaux, Maladie aigüe, Souris.
English descriptors
- KwdEn :
- Acute Disease, Animals, Lung Diseases (enzymology), Lung Diseases (pathology), Mice, Peptidyl-Dipeptidase A (physiology), Pulmonary Edema (genetics), Pulmonary Edema (pathology), Respiratory Distress Syndrome, Adult (genetics), Respiratory Distress Syndrome, Adult (pathology), SARS Virus (pathogenicity), Severe Acute Respiratory Syndrome (genetics), Severe Acute Respiratory Syndrome (pathology).
- MESH :
- chemical , physiology : Peptidyl-Dipeptidase A.
- enzymology : Lung Diseases.
- genetics : Pulmonary Edema, Respiratory Distress Syndrome, Adult, Severe Acute Respiratory Syndrome.
- pathogenicity : SARS Virus.
- pathology : Lung Diseases, Pulmonary Edema, Respiratory Distress Syndrome, Adult, Severe Acute Respiratory Syndrome.
- Acute Disease, Animals, Mice.
Abstract
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.
DOI: 10.1113/expphysiol.2007.040048
PubMed: 18448662
Affiliations:
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Penninger</name></author></analytic><series><title level="j">Experimental physiology</title><idno type="ISSN">0958-0670</idno><imprint><date when="2008" type="published">2008</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acute Disease</term><term>Animals</term><term>Lung Diseases (enzymology)</term><term>Lung Diseases (pathology)</term><term>Mice</term><term>Peptidyl-Dipeptidase A (physiology)</term><term>Pulmonary Edema (genetics)</term><term>Pulmonary Edema (pathology)</term><term>Respiratory Distress Syndrome, Adult (genetics)</term><term>Respiratory Distress Syndrome, Adult (pathology)</term><term>SARS Virus (pathogenicity)</term><term>Severe Acute Respiratory Syndrome (genetics)</term><term>Severe Acute Respiratory Syndrome (pathology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Maladie aigüe</term><term>Maladies pulmonaires (anatomopathologie)</term><term>Maladies pulmonaires (enzymologie)</term><term>Oedème pulmonaire (anatomopathologie)</term><term>Oedème pulmonaire (génétique)</term><term>Peptidyl-Dipeptidase A (physiologie)</term><term>Souris</term><term>Syndrome de détresse respiratoire de l'adulte (anatomopathologie)</term><term>Syndrome de détresse respiratoire de l'adulte (génétique)</term><term>Syndrome respiratoire aigu sévère (anatomopathologie)</term><term>Syndrome respiratoire aigu sévère (génétique)</term><term>Virus du SRAS (pathogénicité)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Peptidyl-Dipeptidase A</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Maladies pulmonaires</term><term>Oedème pulmonaire</term><term>Syndrome de détresse respiratoire de l'adulte</term><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="enzymologie" xml:lang="fr"><term>Maladies pulmonaires</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Lung Diseases</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Pulmonary Edema</term><term>Respiratory Distress Syndrome, Adult</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Oedème pulmonaire</term><term>Syndrome de détresse respiratoire de l'adulte</term><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lung Diseases</term><term>Pulmonary Edema</term><term>Respiratory Distress Syndrome, Adult</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Peptidyl-Dipeptidase A</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Acute Disease</term><term>Animals</term><term>Mice</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Maladie aigüe</term><term>Souris</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">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.</div></front></TEI><affiliations><list><country><li>Japon</li></country></list><tree><noCountry><name sortKey="Kuba, Keiji" sort="Kuba, Keiji" uniqKey="Kuba K" first="Keiji" last="Kuba">Keiji Kuba</name><name sortKey="Penninger, Josef M" sort="Penninger, Josef M" uniqKey="Penninger J" first="Josef M" last="Penninger">Josef M. Penninger</name></noCountry><country name="Japon"><noRegion><name sortKey="Imai, Yumiko" sort="Imai, Yumiko" uniqKey="Imai Y" first="Yumiko" last="Imai">Yumiko Imai</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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