Clinical Implications of SARS-CoV-2 Interaction With Renin Angiotensin System: JACC Review Topic of the Week.
Identifieur interne : 000352 ( Main/Corpus ); précédent : 000351; suivant : 000353Clinical Implications of SARS-CoV-2 Interaction With Renin Angiotensin System: JACC Review Topic of the Week.
Auteurs : Agnieszka Brojakowska ; Jagat Narula ; Rony Shimony ; Jeffrey BanderSource :
- Journal of the American College of Cardiology [ 1558-3597 ] ; 2020.
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
Links to Exploration step
pubmed:32305401Le document en format XML
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Electronic address: jeffrey.bander@mountsinai.org.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2020">2020</date><idno type="RBID">pubmed:32305401</idno><idno type="pmid">32305401</idno><idno type="doi">10.1016/j.jacc.2020.04.028</idno><idno type="pmc">PMC7161517</idno><idno type="wicri:Area/Main/Corpus">000352</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000352</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Clinical Implications of SARS-CoV-2 Interaction With Renin Angiotensin System: JACC Review Topic of the Week.</title><author><name sortKey="Brojakowska, Agnieszka" sort="Brojakowska, Agnieszka" uniqKey="Brojakowska A" first="Agnieszka" last="Brojakowska">Agnieszka Brojakowska</name><affiliation><nlm:affiliation>Department of Cardiology, Icahn School of Medicine at Mount Sinai, New York, New York.</nlm:affiliation></affiliation></author><author><name sortKey="Narula, Jagat" sort="Narula, Jagat" uniqKey="Narula J" first="Jagat" last="Narula">Jagat Narula</name><affiliation><nlm:affiliation>Department of Cardiology, Icahn School of Medicine at Mount Sinai, New York, New York.</nlm:affiliation></affiliation></author><author><name sortKey="Shimony, Rony" sort="Shimony, Rony" uniqKey="Shimony R" first="Rony" last="Shimony">Rony Shimony</name><affiliation><nlm:affiliation>Department of Cardiology, Icahn School of Medicine at Mount Sinai, New York, New York.</nlm:affiliation></affiliation></author><author><name sortKey="Bander, Jeffrey" sort="Bander, Jeffrey" uniqKey="Bander J" first="Jeffrey" last="Bander">Jeffrey Bander</name><affiliation><nlm:affiliation>Department of Cardiology, Icahn School of Medicine at Mount Sinai, New York, New York. Electronic address: jeffrey.bander@mountsinai.org.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Journal of the American College of Cardiology</title><idno type="eISSN">1558-3597</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Angiotensin Receptor Antagonists (pharmacology)</term><term>Angiotensin-Converting Enzyme Inhibitors (pharmacology)</term><term>Betacoronavirus (drug effects)</term><term>Betacoronavirus (physiology)</term><term>Cardiovascular Diseases (drug therapy)</term><term>Cardiovascular Diseases (metabolism)</term><term>Coronavirus Infections (physiopathology)</term><term>Coronavirus 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="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="metabolism" xml:lang="en"><term>Cardiovascular Diseases</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Betacoronavirus</term><term>Renin-Angiotensin System</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="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></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. 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