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SARS-coronavirus modulation of myocardial ACE2 expression and inflammation in patients with SARS.

Identifieur interne : 001896 ( PubMed/Curation ); précédent : 001895; suivant : 001897

SARS-coronavirus modulation of myocardial ACE2 expression and inflammation in patients with SARS.

Auteurs : G Y Oudit [Canada] ; Z. Kassiri ; C. Jiang ; P P Liu ; S M Poutanen ; J M Penninger ; J. Butany

Source :

RBID : pubmed:19453650

Descripteurs français

English descriptors

Abstract

Angiotensin converting enzyme 2 (ACE2), a monocarboxylase that degrades angiotensin II to angiotensin 1-7, is also the functional receptor for severe acute respiratory syndrome (SARS) coronavirus (SARS-CoV) and is highly expressed in the lungs and heart. Patients with SARS also suffered from cardiac disease including arrhythmias, sudden cardiac death, and systolic and diastolic dysfunction.

DOI: 10.1111/j.1365-2362.2009.02153.x
PubMed: 19453650

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pubmed:19453650

Le document en format XML

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<term>Cardiovascular Diseases (virology)</term>
<term>Down-Regulation</term>
<term>Humans</term>
<term>Immunohistochemistry</term>
<term>Male</term>
<term>Mice</term>
<term>Myocardium (pathology)</term>
<term>Peptidyl-Dipeptidase A (genetics)</term>
<term>Peptidyl-Dipeptidase A (metabolism)</term>
<term>SARS Virus (genetics)</term>
<term>SARS Virus (metabolism)</term>
<term>Virus Activation</term>
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<term>Activation virale</term>
<term>Animaux</term>
<term>Autopsie</term>
<term>Humains</term>
<term>Immunohistochimie</term>
<term>Maladies cardiovasculaires ()</term>
<term>Maladies cardiovasculaires (virologie)</term>
<term>Myocarde (anatomopathologie)</term>
<term>Mâle</term>
<term>Peptidyl-Dipeptidase A (génétique)</term>
<term>Peptidyl-Dipeptidase A (métabolisme)</term>
<term>Régulation négative</term>
<term>Souris</term>
<term>Virus du SRAS (génétique)</term>
<term>Virus du SRAS (métabolisme)</term>
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<term>Myocarde</term>
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<term>SARS Virus</term>
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<term>Peptidyl-Dipeptidase A</term>
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<term>SARS Virus</term>
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<term>Peptidyl-Dipeptidase A</term>
<term>Virus du SRAS</term>
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<term>Myocardium</term>
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<term>Cardiovascular Diseases</term>
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<term>Maladies cardiovasculaires</term>
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<term>Cardiovascular Diseases</term>
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<term>Autopsy</term>
<term>Down-Regulation</term>
<term>Humans</term>
<term>Immunohistochemistry</term>
<term>Male</term>
<term>Mice</term>
<term>Virus Activation</term>
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<front>
<div type="abstract" xml:lang="en">Angiotensin converting enzyme 2 (ACE2), a monocarboxylase that degrades angiotensin II to angiotensin 1-7, is also the functional receptor for severe acute respiratory syndrome (SARS) coronavirus (SARS-CoV) and is highly expressed in the lungs and heart. Patients with SARS also suffered from cardiac disease including arrhythmias, sudden cardiac death, and systolic and diastolic dysfunction.</div>
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<DateCompleted>
<Year>2010</Year>
<Month>02</Month>
<Day>22</Day>
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<DateRevised>
<Year>2020</Year>
<Month>04</Month>
<Day>18</Day>
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<ISSN IssnType="Electronic">1365-2362</ISSN>
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<Volume>39</Volume>
<Issue>7</Issue>
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<Year>2009</Year>
<Month>Jul</Month>
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<Title>European journal of clinical investigation</Title>
<ISOAbbreviation>Eur. J. Clin. Invest.</ISOAbbreviation>
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<ArticleTitle>SARS-coronavirus modulation of myocardial ACE2 expression and inflammation in patients with SARS.</ArticleTitle>
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<AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Angiotensin converting enzyme 2 (ACE2), a monocarboxylase that degrades angiotensin II to angiotensin 1-7, is also the functional receptor for severe acute respiratory syndrome (SARS) coronavirus (SARS-CoV) and is highly expressed in the lungs and heart. Patients with SARS also suffered from cardiac disease including arrhythmias, sudden cardiac death, and systolic and diastolic dysfunction.</AbstractText>
<AbstractText Label="MATERIALS AND METHODS" NlmCategory="METHODS">We studied mice infected with the human strain of the SARS-CoV and encephalomyocarditis virus and examined ACE2 mRNA and protein expression. Autopsy heart samples from patients who succumbed to the SARS crisis in Toronto (Canada) were used to investigate the impact of SARS on myocardial structure, inflammation and ACE2 protein expression.</AbstractText>
<AbstractText Label="RESULTS" NlmCategory="RESULTS">Pulmonary infection with the human SARS-CoV in mice led to an ACE2-dependent myocardial infection with a marked decrease in ACE2 expression confirming a critical role of ACE2 in mediating SARS-CoV infection in the heart. The SARS-CoV viral RNA was detected in 35% (7/20) of autopsied human heart samples obtained from patients who succumbed to the SARS crisis during the Toronto SARS outbreak. Macrophage-specific staining showed a marked increase in macrophage infiltration with evidence of myocardial damage in patients who had SARS-CoV in their hearts. The presence of SARS-CoV in the heart was also associated with marked reductions in ACE2 protein expression.</AbstractText>
<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Our data show that SARS-CoV can mediate myocardial inflammation and damage associated with down-regulation of myocardial ACE2 system, which may be responsible for the myocardial dysfunction and adverse cardiac outcomes in patients with SARS.</AbstractText>
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<DescriptorName UI="D007703" MajorTopicYN="N">Peptidyl-Dipeptidase A</DescriptorName>
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