The pivotal link between ACE2 deficiency and SARS-CoV-2 infection.
Identifieur interne : 000337 ( Main/Curation ); précédent : 000336; suivant : 000338The pivotal link between ACE2 deficiency and SARS-CoV-2 infection.
Auteurs : Paolo Verdecchia [Oman] ; Claudio Cavallini ; Antonio Spanevello ; Fabio AngeliSource :
- European journal of internal medicine [ 1879-0828 ] ; 2020.
Descripteurs français
- KwdFr :
- Angiotensines (métabolisme), Antagonistes du récepteur de type 1 de l'angiotensine-II (pharmacologie), Betacoronavirus (effets des médicaments et des substances chimiques), Betacoronavirus (physiologie), Diabète (épidémiologie), Découverte de médicament (MeSH), Défaillance cardiaque (épidémiologie), Facteurs de risque (MeSH), Humains (MeSH), Hypertension artérielle (métabolisme), Infections à coronavirus (immunologie), Infections à coronavirus (métabolisme), Infections à coronavirus (épidémiologie), Pandémies (MeSH), Peptidyl-Dipeptidase A (métabolisme), Pneumopathie virale (immunologie), Pneumopathie virale (métabolisme), Pneumopathie virale (épidémiologie), Protéines recombinantes (pharmacologie), Récepteurs viraux (métabolisme).
- MESH :
- effets des médicaments et des substances chimiques : Betacoronavirus.
- immunologie : Infections à coronavirus, Pneumopathie virale.
- métabolisme : Angiotensines, Hypertension artérielle, Infections à coronavirus, Peptidyl-Dipeptidase A, Pneumopathie virale, Récepteurs viraux.
- pharmacologie : Antagonistes du récepteur de type 1 de l'angiotensine-II, Protéines recombinantes.
- physiologie : Betacoronavirus.
- épidémiologie : Diabète, Défaillance cardiaque, Infections à coronavirus, Pneumopathie virale.
- Découverte de médicament, Facteurs de risque, Humains, Pandémies.
English descriptors
- KwdEn :
- Angiotensin II Type 1 Receptor Blockers (pharmacology), Angiotensins (metabolism), Betacoronavirus (drug effects), Betacoronavirus (physiology), Coronavirus Infections (epidemiology), Coronavirus Infections (immunology), Coronavirus Infections (metabolism), Diabetes Mellitus (epidemiology), Drug Discovery (MeSH), Heart Failure (epidemiology), Humans (MeSH), Hypertension (metabolism), Pandemics (MeSH), Peptidyl-Dipeptidase A (metabolism), Pneumonia, Viral (epidemiology), Pneumonia, Viral (immunology), Pneumonia, Viral (metabolism), Receptors, Virus (metabolism), Recombinant Proteins (pharmacology), Risk Factors (MeSH).
- MESH :
- chemical , metabolism : Angiotensins, Peptidyl-Dipeptidase A, Receptors, Virus.
- chemical , pharmacology : Angiotensin II Type 1 Receptor Blockers, Recombinant Proteins.
- drug effects : Betacoronavirus.
- epidemiology : Coronavirus Infections, Diabetes Mellitus, Heart Failure, Pneumonia, Viral.
- immunology : Coronavirus Infections, Pneumonia, Viral.
- metabolism : Coronavirus Infections, Hypertension, Pneumonia, Viral.
- physiology : Betacoronavirus.
- Drug Discovery, Humans, Pandemics, Risk Factors.
Abstract
Angiotensin converting enzyme-2 (ACE2) receptors mediate the entry into the cell of three strains of coronavirus: SARS-CoV, NL63 and SARS-CoV-2. ACE2 receptors are ubiquitous and widely expressed in the heart, vessels, gut, lung (particularly in type 2 pneumocytes and macrophages), kidney, testis and brain. ACE2 is mostly bound to cell membranes and only scarcely present in the circulation in a soluble form. An important salutary function of membrane-bound and soluble ACE2 is the degradation of angiotensin II to angiotensin1-7. Consequently, ACE2 receptors limit several detrimental effects resulting from binding of angiotensin II to AT1 receptors, which include vasoconstriction, enhanced inflammation and thrombosis. The increased generation of angiotensin1-7 also triggers counter-regulatory protective effects through binding to G-protein coupled Mas receptors. Unfortunately, the entry of SARS-CoV2 into the cells through membrane fusion markedly down-regulates ACE2 receptors, with loss of the catalytic effect of these receptors at the external site of the membrane. Increased pulmonary inflammation and coagulation have been reported as unwanted effects of enhanced and unopposed angiotensin II effects via the ACE→Angiotensin II→AT1 receptor axis. Clinical reports of patients infected with SARS-CoV-2 show that several features associated with infection and severity of the disease (i.e., older age, hypertension, diabetes, cardiovascular disease) share a variable degree of ACE2 deficiency. We suggest that ACE2 down-regulation induced by viral invasion may be especially detrimental in people with baseline ACE2 deficiency associated with the above conditions. The additional ACE2 deficiency after viral invasion might amplify the dysregulation between the 'adverse' ACE→Angiotensin II→AT1 receptor axis and the 'protective' ACE2→Angiotensin1-7→Mas receptor axis. In the lungs, such dysregulation would favor the progression of inflammatory and thrombotic processes triggered by local angiotensin II hyperactivity unopposed by angiotensin1-7. In this setting, recombinant ACE2, angiotensin1-7 and angiotensin II type 1 receptor blockers could be promising therapeutic approaches in patients with SARS-CoV-2 infection.
DOI: 10.1016/j.ejim.2020.04.037
PubMed: 32336612
PubMed Central: PMC7167588
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Claudio Cavallini<affiliation><nlm:affiliation>Fondazione Umbra Cuore e Ipertensione-ONLUS and Struttura Complessa di Cardiologia, Ospedale S. Maria della Misericordia, Perugia.</nlm:affiliation>
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</affiliation>
<affiliation><nlm:affiliation>Dipartimento di Medicina e Chirurgia, Università degli Studi dell'Insubria, Varese; Dipartimento di Medicina e Riabilitazione Cardio-Respiratoria, Istituti Clinici Scientici Maugeri, IRCCS Tradate (VA).</nlm:affiliation>
<wicri:noCountry code="subField">IRCCS Tradate (VA)</wicri:noCountry>
</affiliation>
<affiliation><nlm:affiliation>Dipartimento di Medicina e Chirurgia, Università degli Studi dell'Insubria, Varese; Dipartimento di Medicina e Riabilitazione Cardio-Respiratoria, Istituti Clinici Scientici Maugeri, IRCCS Tradate (VA).</nlm:affiliation>
<wicri:noCountry code="subField">IRCCS Tradate (VA)</wicri:noCountry>
</affiliation>
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<term>Coronavirus Infections (epidemiology)</term>
<term>Coronavirus Infections (immunology)</term>
<term>Coronavirus Infections (metabolism)</term>
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<term>Pandemics (MeSH)</term>
<term>Peptidyl-Dipeptidase A (metabolism)</term>
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<term>Pneumonia, Viral (metabolism)</term>
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<front><div type="abstract" xml:lang="en">Angiotensin converting enzyme-2 (ACE2) receptors mediate the entry into the cell of three strains of coronavirus: SARS-CoV, NL63 and SARS-CoV-2. ACE2 receptors are ubiquitous and widely expressed in the heart, vessels, gut, lung (particularly in type 2 pneumocytes and macrophages), kidney, testis and brain. ACE2 is mostly bound to cell membranes and only scarcely present in the circulation in a soluble form. An important salutary function of membrane-bound and soluble ACE2 is the degradation of angiotensin II to angiotensin<sub>1-7</sub>
. Consequently, ACE2 receptors limit several detrimental effects resulting from binding of angiotensin II to AT1 receptors, which include vasoconstriction, enhanced inflammation and thrombosis. The increased generation of angiotensin<sub>1-7</sub>
also triggers counter-regulatory protective effects through binding to G-protein coupled Mas receptors. Unfortunately, the entry of SARS-CoV2 into the cells through membrane fusion markedly down-regulates ACE2 receptors, with loss of the catalytic effect of these receptors at the external site of the membrane. Increased pulmonary inflammation and coagulation have been reported as unwanted effects of enhanced and unopposed angiotensin II effects via the ACE→Angiotensin II→AT1 receptor axis. Clinical reports of patients infected with SARS-CoV-2 show that several features associated with infection and severity of the disease (i.e., older age, hypertension, diabetes, cardiovascular disease) share a variable degree of ACE2 deficiency. We suggest that ACE2 down-regulation induced by viral invasion may be especially detrimental in people with baseline ACE2 deficiency associated with the above conditions. The additional ACE2 deficiency after viral invasion might amplify the dysregulation between the 'adverse' ACE→Angiotensin II→AT1 receptor axis and the 'protective' ACE2→Angiotensin<sub>1-7</sub>
→Mas receptor axis. In the lungs, such dysregulation would favor the progression of inflammatory and thrombotic processes triggered by local angiotensin II hyperactivity unopposed by angiotensin<sub>1-7</sub>
. In this setting, recombinant ACE2, angiotensin<sub>1-7</sub>
and angiotensin II type 1 receptor blockers could be promising therapeutic approaches in patients with SARS-CoV-2 infection.</div>
</front>
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<Title>European journal of internal medicine</Title>
<ISOAbbreviation>Eur. J. Intern. Med.</ISOAbbreviation>
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<ArticleTitle>The pivotal link between ACE2 deficiency and SARS-CoV-2 infection.</ArticleTitle>
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<Abstract><AbstractText>Angiotensin converting enzyme-2 (ACE2) receptors mediate the entry into the cell of three strains of coronavirus: SARS-CoV, NL63 and SARS-CoV-2. ACE2 receptors are ubiquitous and widely expressed in the heart, vessels, gut, lung (particularly in type 2 pneumocytes and macrophages), kidney, testis and brain. ACE2 is mostly bound to cell membranes and only scarcely present in the circulation in a soluble form. An important salutary function of membrane-bound and soluble ACE2 is the degradation of angiotensin II to angiotensin<sub>1-7</sub>
. Consequently, ACE2 receptors limit several detrimental effects resulting from binding of angiotensin II to AT1 receptors, which include vasoconstriction, enhanced inflammation and thrombosis. The increased generation of angiotensin<sub>1-7</sub>
also triggers counter-regulatory protective effects through binding to G-protein coupled Mas receptors. Unfortunately, the entry of SARS-CoV2 into the cells through membrane fusion markedly down-regulates ACE2 receptors, with loss of the catalytic effect of these receptors at the external site of the membrane. Increased pulmonary inflammation and coagulation have been reported as unwanted effects of enhanced and unopposed angiotensin II effects via the ACE→Angiotensin II→AT1 receptor axis. Clinical reports of patients infected with SARS-CoV-2 show that several features associated with infection and severity of the disease (i.e., older age, hypertension, diabetes, cardiovascular disease) share a variable degree of ACE2 deficiency. We suggest that ACE2 down-regulation induced by viral invasion may be especially detrimental in people with baseline ACE2 deficiency associated with the above conditions. The additional ACE2 deficiency after viral invasion might amplify the dysregulation between the 'adverse' ACE→Angiotensin II→AT1 receptor axis and the 'protective' ACE2→Angiotensin<sub>1-7</sub>
→Mas receptor axis. In the lungs, such dysregulation would favor the progression of inflammatory and thrombotic processes triggered by local angiotensin II hyperactivity unopposed by angiotensin<sub>1-7</sub>
. In this setting, recombinant ACE2, angiotensin<sub>1-7</sub>
and angiotensin II type 1 receptor blockers could be promising therapeutic approaches in patients with SARS-CoV-2 infection.</AbstractText>
<CopyrightInformation>Copyright © 2020 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Verdecchia</LastName>
<ForeName>Paolo</ForeName>
<Initials>P</Initials>
<AffiliationInfo><Affiliation>Fondazione Umbra Cuore e Ipertensione-ONLUS and Struttura Complessa di Cardiologia, Ospedale S. Maria della Misericordia, Perugia.. Electronic address: verdecchiapaolo@gmail.com.</Affiliation>
</AffiliationInfo>
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<ForeName>Claudio</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Fondazione Umbra Cuore e Ipertensione-ONLUS and Struttura Complessa di Cardiologia, Ospedale S. Maria della Misericordia, Perugia.</Affiliation>
</AffiliationInfo>
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<ForeName>Antonio</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Dipartimento di Medicina e Chirurgia, Università degli Studi dell'Insubria, Varese; Dipartimento di Medicina e Riabilitazione Cardio-Respiratoria, Istituti Clinici Scientici Maugeri, IRCCS Tradate (VA).</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Angeli</LastName>
<ForeName>Fabio</ForeName>
<Initials>F</Initials>
<AffiliationInfo><Affiliation>Dipartimento di Medicina e Chirurgia, Università degli Studi dell'Insubria, Varese; Dipartimento di Medicina e Riabilitazione Cardio-Respiratoria, Istituti Clinici Scientici Maugeri, IRCCS Tradate (VA).</Affiliation>
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<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006973" MajorTopicYN="N">Hypertension</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</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="Q000453" MajorTopicYN="N">epidemiology</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011991" MajorTopicYN="N">Receptors, Virus</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011994" MajorTopicYN="N">Recombinant Proteins</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">ACE</Keyword>
<Keyword MajorTopicYN="Y">ACE-inhibitors</Keyword>
<Keyword MajorTopicYN="Y">ACE2</Keyword>
<Keyword MajorTopicYN="Y">Angiotensin receptor blockers</Keyword>
<Keyword MajorTopicYN="Y">Coronavirus</Keyword>
<Keyword MajorTopicYN="Y">Diabetes</Keyword>
<Keyword MajorTopicYN="Y">Elderly</Keyword>
<Keyword MajorTopicYN="Y">Heart failure</Keyword>
<Keyword MajorTopicYN="Y">Hypertension</Keyword>
<Keyword MajorTopicYN="Y">SARS-CoV-2</Keyword>
</KeywordList>
<CoiStatement>Declaration of competing interest The authors declare they have no conflict of interest.</CoiStatement>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2020</Year>
<Month>04</Month>
<Day>13</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2020</Year>
<Month>04</Month>
<Day>16</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2020</Year>
<Month>4</Month>
<Day>28</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2020</Year>
<Month>6</Month>
<Day>19</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2020</Year>
<Month>4</Month>
<Day>28</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">32336612</ArticleId>
<ArticleId IdType="pii">S0953-6205(20)30151-5</ArticleId>
<ArticleId IdType="doi">10.1016/j.ejim.2020.04.037</ArticleId>
<ArticleId IdType="pmc">PMC7167588</ArticleId>
</ArticleIdList>
</PubmedData>
</pubmed>
</record>
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