Interactions of coronaviruses with ACE2, angiotensin II, and RAS inhibitors-lessons from available evidence and insights into COVID-19.
Identifieur interne : 000334 ( Main/Corpus ); précédent : 000333; suivant : 000335Interactions of coronaviruses with ACE2, angiotensin II, and RAS inhibitors-lessons from available evidence and insights into COVID-19.
Auteurs : Hisashi Kai ; Mamiko KaiSource :
- Hypertension research : official journal of the Japanese Society of Hypertension [ 1348-4214 ] ; 2020.
English descriptors
- KwdEn :
- Angiotensin II (physiology), Angiotensin Receptor Antagonists (adverse effects), Angiotensin-Converting Enzyme Inhibitors (adverse effects), Animals (MeSH), Betacoronavirus (MeSH), Coronavirus Infections (etiology), Humans (MeSH), Pandemics (MeSH), Peptidyl-Dipeptidase A (physiology), Pneumonia, Viral (etiology).
- MESH :
- chemical , adverse effects : Angiotensin Receptor Antagonists, Angiotensin-Converting Enzyme Inhibitors.
- chemical , physiology : Angiotensin II, Peptidyl-Dipeptidase A.
- etiology : Coronavirus Infections, Pneumonia, Viral.
- Animals, Betacoronavirus, Humans, Pandemics.
Abstract
The rapid spread of a novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has led to an ongoing pandemic of coronavirus disease 2019 (COVID-19). Recently, angiotensin-converting enzyme 2 (ACE2) has been shown to be a functional receptor for SARS-CoV-2 to enter host target cells. Given that angiotensin receptor blockers (ARBs) and an ACE inhibitor (ACEI) upregulated ACE2 expression in animal studies, the concern might arise regarding whether ARBs and ACEIs would increase the morbidity and mortality of COVID-19. On the other hand, animal data suggested a potential protective effect of ARBs against COVID-19 pneumonia because an ARB prevented the aggravation of acute lung injury in mice infected with SARS-CoV, which is closely related to SARS-CoV-2. Importantly, however, there is no clinical or experimental evidence supporting that ARBs and ACEIs either augment the susceptibility to SARS-CoV-2 or aggravate the severity and outcomes of COVID-19 at present. Until further data are available, it is recommended that ARB and ACEI medications be continued for the treatment of patients with cardiovascular disease and hypertension, especially those at high risk, according to guideline-directed medical therapy based on the currently available evidence.
DOI: 10.1038/s41440-020-0455-8
PubMed: 32341442
PubMed Central: PMC7184165
Links to Exploration step
pubmed:32341442Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Interactions of coronaviruses with ACE2, angiotensin II, and RAS inhibitors-lessons from available evidence and insights into COVID-19.</title><author><name sortKey="Kai, Hisashi" sort="Kai, Hisashi" uniqKey="Kai H" first="Hisashi" last="Kai">Hisashi Kai</name><affiliation><nlm:affiliation>Department of Cardiology, Kurume University Medical Center, Kurume, Japan. naikai@med.kurume-u.ac.jp.</nlm:affiliation></affiliation></author><author><name sortKey="Kai, Mamiko" sort="Kai, Mamiko" uniqKey="Kai M" first="Mamiko" last="Kai">Mamiko Kai</name><affiliation><nlm:affiliation>Department of Pharmaceutical and Health Care Management, Faculty of Pharmaceutical Sciences, Fukuoka University, Fukuoka, Japan.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2020">2020</date><idno type="RBID">pubmed:32341442</idno><idno type="pmid">32341442</idno><idno type="doi">10.1038/s41440-020-0455-8</idno><idno type="pmc">PMC7184165</idno><idno type="wicri:Area/Main/Corpus">000334</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000334</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Interactions of coronaviruses with ACE2, angiotensin II, and RAS inhibitors-lessons from available evidence and insights into COVID-19.</title><author><name sortKey="Kai, Hisashi" sort="Kai, Hisashi" uniqKey="Kai H" first="Hisashi" last="Kai">Hisashi Kai</name><affiliation><nlm:affiliation>Department of Cardiology, Kurume University Medical Center, Kurume, Japan. naikai@med.kurume-u.ac.jp.</nlm:affiliation></affiliation></author><author><name sortKey="Kai, Mamiko" sort="Kai, Mamiko" uniqKey="Kai M" first="Mamiko" last="Kai">Mamiko Kai</name><affiliation><nlm:affiliation>Department of Pharmaceutical and Health Care Management, Faculty of Pharmaceutical Sciences, Fukuoka University, Fukuoka, Japan.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Hypertension research : official journal of the Japanese Society of Hypertension</title><idno type="eISSN">1348-4214</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Angiotensin II (physiology)</term><term>Angiotensin Receptor Antagonists (adverse effects)</term><term>Angiotensin-Converting Enzyme Inhibitors (adverse effects)</term><term>Animals (MeSH)</term><term>Betacoronavirus (MeSH)</term><term>Coronavirus Infections (etiology)</term><term>Humans (MeSH)</term><term>Pandemics (MeSH)</term><term>Peptidyl-Dipeptidase A (physiology)</term><term>Pneumonia, Viral (etiology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Angiotensin Receptor Antagonists</term><term>Angiotensin-Converting Enzyme Inhibitors</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Angiotensin II</term><term>Peptidyl-Dipeptidase A</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Coronavirus Infections</term><term>Pneumonia, Viral</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Betacoronavirus</term><term>Humans</term><term>Pandemics</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The rapid spread of a novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has led to an ongoing pandemic of coronavirus disease 2019 (COVID-19). Recently, angiotensin-converting enzyme 2 (ACE2) has been shown to be a functional receptor for SARS-CoV-2 to enter host target cells. Given that angiotensin receptor blockers (ARBs) and an ACE inhibitor (ACEI) upregulated ACE2 expression in animal studies, the concern might arise regarding whether ARBs and ACEIs would increase the morbidity and mortality of COVID-19. On the other hand, animal data suggested a potential protective effect of ARBs against COVID-19 pneumonia because an ARB prevented the aggravation of acute lung injury in mice infected with SARS-CoV, which is closely related to SARS-CoV-2. Importantly, however, there is no clinical or experimental evidence supporting that ARBs and ACEIs either augment the susceptibility to SARS-CoV-2 or aggravate the severity and outcomes of COVID-19 at present. Until further data are available, it is recommended that ARB and ACEI medications be continued for the treatment of patients with cardiovascular disease and hypertension, especially those at high risk, according to guideline-directed medical therapy based on the currently available evidence.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">32341442</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">1348-4214</ISSN><JournalIssue CitedMedium="Internet"><Volume>43</Volume><Issue>7</Issue><PubDate><Year>2020</Year><Month>07</Month></PubDate></JournalIssue><Title>Hypertension research : official journal of the Japanese Society of Hypertension</Title><ISOAbbreviation>Hypertens. Res.</ISOAbbreviation></Journal><ArticleTitle>Interactions of coronaviruses with ACE2, angiotensin II, and RAS inhibitors-lessons from available evidence and insights into COVID-19.</ArticleTitle><Pagination><MedlinePgn>648-654</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/s41440-020-0455-8</ELocationID><Abstract><AbstractText>The rapid spread of a novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has led to an ongoing pandemic of coronavirus disease 2019 (COVID-19). Recently, angiotensin-converting enzyme 2 (ACE2) has been shown to be a functional receptor for SARS-CoV-2 to enter host target cells. Given that angiotensin receptor blockers (ARBs) and an ACE inhibitor (ACEI) upregulated ACE2 expression in animal studies, the concern might arise regarding whether ARBs and ACEIs would increase the morbidity and mortality of COVID-19. On the other hand, animal data suggested a potential protective effect of ARBs against COVID-19 pneumonia because an ARB prevented the aggravation of acute lung injury in mice infected with SARS-CoV, which is closely related to SARS-CoV-2. Importantly, however, there is no clinical or experimental evidence supporting that ARBs and ACEIs either augment the susceptibility to SARS-CoV-2 or aggravate the severity and outcomes of COVID-19 at present. Until further data are available, it is recommended that ARB and ACEI medications be continued for the treatment of patients with cardiovascular disease and hypertension, especially those at high risk, according to guideline-directed medical therapy based on the currently available evidence.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kai</LastName><ForeName>Hisashi</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Cardiology, Kurume University Medical Center, Kurume, Japan. naikai@med.kurume-u.ac.jp.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kai</LastName><ForeName>Mamiko</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Pharmaceutical and Health Care Management, Faculty of Pharmaceutical Sciences, Fukuoka University, Fukuoka, Japan.</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>27</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Hypertens Res</MedlineTA><NlmUniqueID>9307690</NlmUniqueID><ISSNLinking>0916-9636</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>11128-99-7</RegistryNumber><NameOfSubstance UI="D000804">Angiotensin II</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>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000804" MajorTopicYN="N">Angiotensin II</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D057911" MajorTopicYN="N">Angiotensin Receptor Antagonists</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="Y">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000806" MajorTopicYN="N">Angiotensin-Converting Enzyme Inhibitors</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="Y">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000073640" MajorTopicYN="Y">Betacoronavirus</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018352" MajorTopicYN="N">Coronavirus Infections</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D058873" MajorTopicYN="N">Pandemics</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007703" MajorTopicYN="N">Peptidyl-Dipeptidase A</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011024" MajorTopicYN="N">Pneumonia, Viral</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Acute lung injury</Keyword><Keyword MajorTopicYN="Y">Angiotensin II type-1 receptor</Keyword><Keyword MajorTopicYN="Y">Angiotensin receptor blocker</Keyword><Keyword MajorTopicYN="Y">Angiotensin-converting enzyme inhibitor</Keyword><Keyword MajorTopicYN="Y">Severe acute respiratory syndrome coronavirus 2</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2020</Year><Month>04</Month><Day>06</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2020</Year><Month>04</Month><Day>09</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2020</Year><Month>04</Month><Day>08</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>4</Month><Day>29</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>7</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>4</Month><Day>29</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32341442</ArticleId><ArticleId IdType="doi">10.1038/s41440-020-0455-8</ArticleId><ArticleId IdType="pii">10.1038/s41440-020-0455-8</ArticleId><ArticleId IdType="pmc">PMC7184165</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Sante/explor/CardioCovidV1/Data/Main/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000334 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Corpus/biblio.hfd -nk 000334 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Sante
|area= CardioCovidV1
|flux= Main
|étape= Corpus
|type= RBID
|clé= pubmed:32341442
|texte= Interactions of coronaviruses with ACE2, angiotensin II, and RAS inhibitors-lessons from available evidence and insights into COVID-19.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Corpus/RBID.i -Sk "pubmed:32341442" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Corpus/biblio.hfd \
| NlmPubMed2Wicri -a CardioCovidV1
| This area was generated with Dilib version V0.6.35. |  |