Lessons from SARS: control of acute lung failure by the SARS receptor ACE2
Identifieur interne : 004238 ( Main/Exploration ); précédent : 004237; suivant : 004239Lessons from SARS: control of acute lung failure by the SARS receptor ACE2
Auteurs : Keiji Kuba [Autriche] ; Yumiko Imai [Autriche] ; Shuan Rao [République populaire de Chine] ; Chengyu Jiang [République populaire de Chine] ; Josef M. Penninger [Autriche]Source :
- Journal of Molecular Medicine [ 0946-2716 ] ; 2006-10-01.
Descripteurs français
- KwdFr :
- Animaux, Humains, Maladies cardiovasculaires (), Maladies cardiovasculaires (enzymologie), Maladies cardiovasculaires (métabolisme), Maladies pulmonaires (), Maladies pulmonaires (enzymologie), Maladies pulmonaires (métabolisme), Modèles biologiques, Peptidyl-Dipeptidase A (génétique), Peptidyl-Dipeptidase A (métabolisme), Souris, Syndrome respiratoire aigu sévère (enzymologie), Syndrome respiratoire aigu sévère (métabolisme), Syndrome respiratoire aigu sévère (virologie), Thérapie génétique (), Virus du SRAS (croissance et développement), Virus du SRAS (métabolisme).
- MESH :
- croissance et développement : Virus du SRAS.
- enzymologie : Maladies cardiovasculaires, Maladies pulmonaires, Syndrome respiratoire aigu sévère.
- génétique : Peptidyl-Dipeptidase A.
- métabolisme : Maladies cardiovasculaires, Maladies pulmonaires, Peptidyl-Dipeptidase A, Syndrome respiratoire aigu sévère, Virus du SRAS.
- virologie : Syndrome respiratoire aigu sévère.
- Animaux, Humains, Maladies cardiovasculaires, Maladies pulmonaires, Modèles biologiques, Souris, Thérapie génétique.
- Pascal (Inist)
- Wicri :
- topic : Médecine.
English descriptors
- KwdEn :
- Acute, Acute respiratory distress syndrome, Angiotensin-converting enzyme 2, Animal, Animals, Biological receptor, Cardiovascular Diseases (enzymology), Cardiovascular Diseases (metabolism), Cardiovascular Diseases (therapy), Coronavirus, Genetic Therapy (methods), Humans, Knockout mice, Knockout mouse, Lung Diseases (enzymology), Lung Diseases (metabolism), Lung Diseases (therapy), Medicine, Mice, Models, Biological, Peptidyl-Dipeptidase A (genetics), Peptidyl-Dipeptidase A (metabolism), Peptidyl-dipeptidase A, Renin angiotensin system, Renin–angiotensin system, Respiratory distress, SARS Virus (growth & development), SARS Virus (metabolism), SARS coronavirus, Severe Acute Respiratory Syndrome (enzymology), Severe Acute Respiratory Syndrome (metabolism), Severe Acute Respiratory Syndrome (virology), Severe acute respiratory syndrome.
- MESH :
- chemical , genetics : Peptidyl-Dipeptidase A.
- enzymology : Cardiovascular Diseases, Lung Diseases, Severe Acute Respiratory Syndrome.
- growth & development : SARS Virus.
- metabolism : Cardiovascular Diseases, Lung Diseases, Peptidyl-Dipeptidase A, SARS Virus, Severe Acute Respiratory Syndrome.
- methods : Genetic Therapy.
- therapy : Cardiovascular Diseases, Lung Diseases.
- virology : Severe Acute Respiratory Syndrome.
- Animals, Humans, Mice, Models, Biological.
Abstract
Abstract: Angiotensin-converting enzyme 2 (ACE2), a second angiotensin-converting enzyme (ACE), regulates the renin–angiotensin system by counterbalancing ACE activity. Accumulating evidence in recent years has demonstrated a physiological and pathological role of ACE2 in the cardiovascular systems. Recently, it has been shown that severe acute respiratory syndrome (SARS) coronavirus, the cause of SARS, utilizes ACE2 as an essential receptor for cell fusion and in vivo infections in mice. Intriguingly, ACE2 acts as a protective factor in various experimental models of acute lung failure and, therefore, acts not only as a key determinant for SARS virus entry into cells but also contributes to SARS pathogenesis. Here we review the role of ACE2 in disease pathogenesis, including lung diseases and cardiovascular diseases.
Url:
DOI: 10.1007/s00109-006-0094-9
Affiliations:
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Le document en format XML
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ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Angiotensin-converting enzyme 2 (ACE2), a second angiotensin-converting enzyme (ACE), regulates the renin–angiotensin system by counterbalancing ACE activity. Accumulating evidence in recent years has demonstrated a physiological and pathological role of ACE2 in the cardiovascular systems. Recently, it has been shown that severe acute respiratory syndrome (SARS) coronavirus, the cause of SARS, utilizes ACE2 as an essential receptor for cell fusion and in vivo infections in mice. Intriguingly, ACE2 acts as a protective factor in various experimental models of acute lung failure and, therefore, acts not only as a key determinant for SARS virus entry into cells but also contributes to SARS pathogenesis. Here we review the role of ACE2 in disease pathogenesis, including lung diseases and cardiovascular diseases.</div></front></TEI><affiliations><list><country><li>Autriche</li><li>République populaire de Chine</li></country><region><li>Vienne (Autriche)</li></region><settlement><li>Pékin</li><li>Vienne (Autriche)</li></settlement></list><tree><country name="Autriche"><region name="Vienne (Autriche)"><name sortKey="Kuba, Keiji" sort="Kuba, Keiji" uniqKey="Kuba K" first="Keiji" last="Kuba">Keiji Kuba</name></region><name sortKey="Imai, Yumiko" sort="Imai, Yumiko" uniqKey="Imai Y" first="Yumiko" last="Imai">Yumiko Imai</name><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><name sortKey="Penninger, Josef M" sort="Penninger, Josef M" uniqKey="Penninger J" first="Josef M." last="Penninger">Josef M. Penninger</name></country><country name="République populaire de Chine"><noRegion><name sortKey="Rao, Shuan" sort="Rao, Shuan" uniqKey="Rao S" first="Shuan" last="Rao">Shuan Rao</name></noRegion><name sortKey="Jiang, Chengyu" sort="Jiang, Chengyu" uniqKey="Jiang C" first="Chengyu" last="Jiang">Chengyu Jiang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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