Clinical Implications of SARS-CoV-2 Interaction With Renin Angiotensin System: JACC Review Topic of the Week.
Identifieur interne : 000276 ( Main/Exploration ); précédent : 000275; suivant : 000277Clinical Implications of SARS-CoV-2 Interaction With Renin Angiotensin System: JACC Review Topic of the Week.
Auteurs : Agnieszka Brojakowska [États-Unis] ; Jagat Narula [États-Unis] ; Rony Shimony [États-Unis] ; Jeffrey Bander [États-Unis]Source :
- Journal of the American College of Cardiology [ 1558-3597 ] ; 2020.
Descripteurs français
- KwdFr :
- Antagonistes des récepteurs aux angiotensines (pharmacologie), Antagonistes des récepteurs des minéralocorticoïdes (pharmacologie), Betacoronavirus (effets des médicaments et des substances chimiques), Betacoronavirus (physiologie), Gestion de la pharmacothérapie (MeSH), Humains (MeSH), Infections à coronavirus (physiopathologie), Infections à coronavirus (thérapie), Infections à coronavirus (virologie), Inhibiteurs de l'enzyme de conversion de l'angiotensine (pharmacologie), Interactions hôte-microbes (effets des médicaments et des substances chimiques), Maladies cardiovasculaires (métabolisme), Maladies cardiovasculaires (traitement médicamenteux), Pandémies (MeSH), Peptidyl-Dipeptidase A (métabolisme), Pneumopathie virale (physiopathologie), Pneumopathie virale (thérapie), Pneumopathie virale (virologie), Système rénine-angiotensine (effets des médicaments et des substances chimiques), Système rénine-angiotensine (physiologie).
- MESH :
- effets des médicaments et des substances chimiques : Betacoronavirus, Interactions hôte-microbes, Système rénine-angiotensine.
- métabolisme : Maladies cardiovasculaires, Peptidyl-Dipeptidase A.
- pharmacologie : Antagonistes des récepteurs aux angiotensines, Antagonistes des récepteurs des minéralocorticoïdes, Inhibiteurs de l'enzyme de conversion de l'angiotensine.
- physiologie : Betacoronavirus, Système rénine-angiotensine.
- physiopathologie : Infections à coronavirus, Pneumopathie virale.
- thérapie : Infections à coronavirus, Pneumopathie virale.
- traitement médicamenteux : Maladies cardiovasculaires.
- virologie : Infections à coronavirus, Pneumopathie virale.
- Gestion de la pharmacothérapie, Humains, Pandémies.
English descriptors
- KwdEn :
- Angiotensin Receptor Antagonists (pharmacology), Angiotensin-Converting Enzyme Inhibitors (pharmacology), Betacoronavirus (drug effects), Betacoronavirus (physiology), Cardiovascular Diseases (drug therapy), Cardiovascular Diseases (metabolism), Coronavirus Infections (physiopathology), Coronavirus Infections (therapy), Coronavirus Infections (virology), Host Microbial Interactions (drug effects), Humans (MeSH), Medication Therapy Management (MeSH), Mineralocorticoid Receptor Antagonists (pharmacology), Pandemics (MeSH), Peptidyl-Dipeptidase A (metabolism), Pneumonia, Viral (physiopathology), Pneumonia, Viral (therapy), Pneumonia, Viral (virology), Renin-Angiotensin System (drug effects), Renin-Angiotensin System (physiology).
- MESH :
- chemical , metabolism : Peptidyl-Dipeptidase A.
- chemical , pharmacology : Angiotensin Receptor Antagonists, Angiotensin-Converting Enzyme Inhibitors, Mineralocorticoid Receptor Antagonists.
- drug effects : Betacoronavirus, Host Microbial Interactions, Renin-Angiotensin System.
- drug therapy : Cardiovascular Diseases.
- metabolism : Cardiovascular Diseases.
- physiology : Betacoronavirus, Renin-Angiotensin System.
- physiopathology : Coronavirus Infections, Pneumonia, Viral.
- therapy : Coronavirus Infections, Pneumonia, Viral.
- virology : Coronavirus Infections, Pneumonia, Viral.
- Humans, Medication Therapy Management, Pandemics.
Abstract
Severe acute respiratory-syndrome coronavirus-2 (SARS-CoV-2) host cell infection is mediated by binding to angiotensin-converting enzyme 2 (ACE2). Systemic dysregulation observed in SARS-CoV was previously postulated to be due to ACE2/angiotensin 1-7 (Ang1-7)/Mas axis downregulation; increased ACE2 activity was shown to mediate disease protection. Because angiotensin II receptor blockers, ACE inhibitors, and mineralocorticoid receptor antagonists increase ACE2 receptor expression, it has been tacitly believed that the use of these agents may facilitate viral disease; thus, they should not be used in high-risk patients with cardiovascular disease. Based on the anti-inflammatory benefits of the upregulation of the ACE2/Ang1-7/Mas axis and previously demonstrated benefits of lung function improvement in SARS-CoV infections, it has been hypothesized that the benefits of treatment with renin-angiotensin system inhibitors in SARS-CoV-2 may outweigh the risks and at the very least should not be withheld.
DOI: 10.1016/j.jacc.2020.04.028
PubMed: 32305401
PubMed Central: PMC7161517
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Infections (therapy)</term><term>Coronavirus Infections (virology)</term><term>Host Microbial Interactions (drug effects)</term><term>Humans (MeSH)</term><term>Medication Therapy Management (MeSH)</term><term>Mineralocorticoid Receptor Antagonists (pharmacology)</term><term>Pandemics (MeSH)</term><term>Peptidyl-Dipeptidase A (metabolism)</term><term>Pneumonia, Viral (physiopathology)</term><term>Pneumonia, Viral (therapy)</term><term>Pneumonia, Viral (virology)</term><term>Renin-Angiotensin System (drug effects)</term><term>Renin-Angiotensin System (physiology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Antagonistes des récepteurs aux angiotensines (pharmacologie)</term><term>Antagonistes des récepteurs des minéralocorticoïdes (pharmacologie)</term><term>Betacoronavirus (effets des médicaments et des substances chimiques)</term><term>Betacoronavirus (physiologie)</term><term>Gestion de la pharmacothérapie (MeSH)</term><term>Humains (MeSH)</term><term>Infections à coronavirus (physiopathologie)</term><term>Infections à coronavirus (thérapie)</term><term>Infections à coronavirus (virologie)</term><term>Inhibiteurs de l'enzyme de conversion de l'angiotensine (pharmacologie)</term><term>Interactions hôte-microbes (effets des médicaments et des substances chimiques)</term><term>Maladies cardiovasculaires (métabolisme)</term><term>Maladies cardiovasculaires (traitement médicamenteux)</term><term>Pandémies (MeSH)</term><term>Peptidyl-Dipeptidase A (métabolisme)</term><term>Pneumopathie virale (physiopathologie)</term><term>Pneumopathie virale (thérapie)</term><term>Pneumopathie virale (virologie)</term><term>Système rénine-angiotensine (effets des médicaments et des substances chimiques)</term><term>Système rénine-angiotensine (physiologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Peptidyl-Dipeptidase A</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Angiotensin Receptor Antagonists</term><term>Angiotensin-Converting Enzyme Inhibitors</term><term>Mineralocorticoid Receptor Antagonists</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Betacoronavirus</term><term>Host Microbial Interactions</term><term>Renin-Angiotensin System</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Cardiovascular Diseases</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Betacoronavirus</term><term>Interactions hôte-microbes</term><term>Système rénine-angiotensine</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Cardiovascular Diseases</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Maladies cardiovasculaires</term><term>Peptidyl-Dipeptidase A</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antagonistes des récepteurs aux angiotensines</term><term>Antagonistes des récepteurs des minéralocorticoïdes</term><term>Inhibiteurs de l'enzyme de conversion de l'angiotensine</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Betacoronavirus</term><term>Système rénine-angiotensine</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Betacoronavirus</term><term>Renin-Angiotensin System</term></keywords><keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Infections à coronavirus</term><term>Pneumopathie virale</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Coronavirus Infections</term><term>Pneumonia, Viral</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Coronavirus Infections</term><term>Pneumonia, Viral</term></keywords><keywords scheme="MESH" qualifier="thérapie" xml:lang="fr"><term>Infections à coronavirus</term><term>Pneumopathie virale</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Maladies cardiovasculaires</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Infections à coronavirus</term><term>Pneumopathie virale</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Coronavirus Infections</term><term>Pneumonia, Viral</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Humans</term><term>Medication Therapy Management</term><term>Pandemics</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Gestion de la pharmacothérapie</term><term>Humains</term><term>Pandémies</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Severe acute respiratory-syndrome coronavirus-2 (SARS-CoV-2) host cell infection is mediated by binding to angiotensin-converting enzyme 2 (ACE2). Systemic dysregulation observed in SARS-CoV was previously postulated to be due to ACE2/angiotensin 1-7 (Ang1-7)/Mas axis downregulation; increased ACE2 activity was shown to mediate disease protection. Because angiotensin II receptor blockers, ACE inhibitors, and mineralocorticoid receptor antagonists increase ACE2 receptor expression, it has been tacitly believed that the use of these agents may facilitate viral disease; thus, they should not be used in high-risk patients with cardiovascular disease. Based on the anti-inflammatory benefits of the upregulation of the ACE2/Ang1-7/Mas axis and previously demonstrated benefits of lung function improvement in SARS-CoV infections, it has been hypothesized that the benefits of treatment with renin-angiotensin system inhibitors in SARS-CoV-2 may outweigh the risks and at the very least should not be withheld.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">32305401</PMID><DateCompleted><Year>2020</Year><Month>06</Month><Day>29</Day></DateCompleted><DateRevised><Year>2020</Year><Month>06</Month><Day>29</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1558-3597</ISSN><JournalIssue CitedMedium="Internet"><Volume>75</Volume><Issue>24</Issue><PubDate><Year>2020</Year><Month>06</Month><Day>23</Day></PubDate></JournalIssue><Title>Journal of the American College of Cardiology</Title><ISOAbbreviation>J. Am. Coll. Cardiol.</ISOAbbreviation></Journal><ArticleTitle>Clinical Implications of SARS-CoV-2 Interaction With Renin Angiotensin System: JACC Review Topic of the Week.</ArticleTitle><Pagination><MedlinePgn>3085-3095</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0735-1097(20)35001-4</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.jacc.2020.04.028</ELocationID><Abstract><AbstractText>Severe acute respiratory-syndrome coronavirus-2 (SARS-CoV-2) host cell infection is mediated by binding to angiotensin-converting enzyme 2 (ACE2). Systemic dysregulation observed in SARS-CoV was previously postulated to be due to ACE2/angiotensin 1-7 (Ang1-7)/Mas axis downregulation; increased ACE2 activity was shown to mediate disease protection. Because angiotensin II receptor blockers, ACE inhibitors, and mineralocorticoid receptor antagonists increase ACE2 receptor expression, it has been tacitly believed that the use of these agents may facilitate viral disease; thus, they should not be used in high-risk patients with cardiovascular disease. Based on the anti-inflammatory benefits of the upregulation of the ACE2/Ang1-7/Mas axis and previously demonstrated benefits of lung function improvement in SARS-CoV infections, it has been hypothesized that the benefits of treatment with renin-angiotensin system inhibitors in SARS-CoV-2 may outweigh the risks and at the very least should not be withheld.</AbstractText><CopyrightInformation>Copyright © 2020. Published by Elsevier Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Brojakowska</LastName><ForeName>Agnieszka</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Icahn School of Medicine at Mount Sinai, New York, New York.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Narula</LastName><ForeName>Jagat</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Icahn School of Medicine at Mount Sinai, New York, New York.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shimony</LastName><ForeName>Rony</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Icahn School of Medicine at Mount Sinai, New York, New York.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bander</LastName><ForeName>Jeffrey</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Icahn School of Medicine at Mount Sinai, New York, New York. Electronic address: jeffrey.bander@mountsinai.org.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>04</Month><Day>16</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Am Coll Cardiol</MedlineTA><NlmUniqueID>8301365</NlmUniqueID><ISSNLinking>0735-1097</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D057911">Angiotensin Receptor Antagonists</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000806">Angiotensin-Converting Enzyme Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000451">Mineralocorticoid Receptor Antagonists</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.15.1</RegistryNumber><NameOfSubstance UI="D007703">Peptidyl-Dipeptidase A</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.17.-</RegistryNumber><NameOfSubstance UI="C413524">angiotensin converting enzyme 2</NameOfSubstance></Chemical></ChemicalList><SupplMeshList><SupplMeshName Type="Disease" UI="C000657245">COVID-19</SupplMeshName><SupplMeshName Type="Organism" UI="C000656484">severe acute respiratory syndrome coronavirus 2</SupplMeshName></SupplMeshList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D057911" MajorTopicYN="N">Angiotensin Receptor Antagonists</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000806" MajorTopicYN="N">Angiotensin-Converting Enzyme Inhibitors</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000073640" MajorTopicYN="Y">Betacoronavirus</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002318" MajorTopicYN="Y">Cardiovascular Diseases</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018352" MajorTopicYN="Y">Coronavirus Infections</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000076662" MajorTopicYN="N">Host Microbial Interactions</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D054539" MajorTopicYN="N">Medication Therapy Management</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000451" MajorTopicYN="N">Mineralocorticoid Receptor Antagonists</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D058873" MajorTopicYN="Y">Pandemics</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007703" MajorTopicYN="N">Peptidyl-Dipeptidase A</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011024" MajorTopicYN="Y">Pneumonia, Viral</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012084" MajorTopicYN="N">Renin-Angiotensin System</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">ACE inhibitor</Keyword><Keyword MajorTopicYN="Y">COVID-19</Keyword><Keyword MajorTopicYN="Y">SARS-CoV-2</Keyword><Keyword MajorTopicYN="Y">angiotensin II receptor blockers</Keyword><Keyword MajorTopicYN="Y">angiotensin-converting enzyme-2</Keyword><Keyword MajorTopicYN="Y">mineralocorticoid receptor antagonist</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2020</Year><Month>04</Month><Day>02</Day></PubMedPubDate><PubMedPubDate 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York</li></region></list><tree><country name="États-Unis"><region name="État de New York"><name sortKey="Brojakowska, Agnieszka" sort="Brojakowska, Agnieszka" uniqKey="Brojakowska A" first="Agnieszka" last="Brojakowska">Agnieszka Brojakowska</name></region><name sortKey="Bander, Jeffrey" sort="Bander, Jeffrey" uniqKey="Bander J" first="Jeffrey" last="Bander">Jeffrey Bander</name><name sortKey="Narula, Jagat" sort="Narula, Jagat" uniqKey="Narula J" first="Jagat" last="Narula">Jagat Narula</name><name sortKey="Shimony, Rony" sort="Shimony, Rony" uniqKey="Shimony R" first="Rony" last="Shimony">Rony Shimony</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd \
| NlmPubMed2Wicri -a CardioCovidV1
| This area was generated with Dilib version V0.6.35. |  |