Renin-angiotensin system at the heart of COVID-19 pandemic.
Identifieur interne : 000769 ( Main/Exploration ); précédent : 000768; suivant : 000770Renin-angiotensin system at the heart of COVID-19 pandemic.
Auteurs : Marco Alifano [France] ; Pietro Alifano [Italie] ; Patricia Forgez [France] ; Antonio Iannelli [France]Source :
- Biochimie [ 1638-6183 ] ; 2020.
Descripteurs français
- KwdFr :
- Adulte d'âge moyen (MeSH), Betacoronavirus (MeSH), Facteurs de risque (MeSH), Femelle (MeSH), Humains (MeSH), Hypertension artérielle (complications), Infections à coronavirus (complications), Infections à coronavirus (métabolisme), Infections à coronavirus (physiopathologie), Maladies cardiovasculaires (complications), Mâle (MeSH), Pandémies (MeSH), Peptidyl-Dipeptidase A (génétique), Peptidyl-Dipeptidase A (métabolisme), Pneumopathie virale (complications), Pneumopathie virale (métabolisme), Pneumopathie virale (physiopathologie), Sujet âgé (MeSH), Système rénine-angiotensine (physiologie).
- MESH :
- génétique : Hypertension artérielle, Infections à coronavirus, Maladies cardiovasculaires, Peptidyl-Dipeptidase A, Pneumopathie virale.
- métabolisme : Infections à coronavirus, Peptidyl-Dipeptidase A, Pneumopathie virale.
- physiologie : Système rénine-angiotensine.
- physiopathologie : Infections à coronavirus, Pneumopathie virale.
- Adulte d'âge moyen, Betacoronavirus, Facteurs de risque, Femelle, Humains, Mâle, Pandémies, Sujet âgé.
English descriptors
- KwdEn :
- Aged (MeSH), Betacoronavirus (MeSH), Cardiovascular Diseases (complications), Coronavirus Infections (complications), Coronavirus Infections (metabolism), Coronavirus Infections (physiopathology), Female (MeSH), Humans (MeSH), Hypertension (complications), Male (MeSH), Middle Aged (MeSH), Pandemics (MeSH), Peptidyl-Dipeptidase A (genetics), Peptidyl-Dipeptidase A (metabolism), Pneumonia, Viral (complications), Pneumonia, Viral (metabolism), Pneumonia, Viral (physiopathology), Renin-Angiotensin System (physiology), Risk Factors (MeSH).
- MESH :
- chemical , genetics : Peptidyl-Dipeptidase A.
- complications : Cardiovascular Diseases, Coronavirus Infections, Hypertension, Pneumonia, Viral.
- metabolism : Coronavirus Infections, Peptidyl-Dipeptidase A, Pneumonia, Viral.
- physiology : Renin-Angiotensin System.
- physiopathology : Coronavirus Infections, Pneumonia, Viral.
- Aged, Betacoronavirus, Female, Humans, Male, Middle Aged, Pandemics, Risk Factors.
Abstract
Significant aspects of COVID-19 pandemic remain obscure. Angiotensin converting enzyme 2 (ACE2), a component of the renin-angiotensin system, whose expression dominates on lung alveolar epithelial cells, is the human cell receptor of SARS-CoV-2, the causative agent of COVID-19. We strongly encourage the concept that thorough considerations of receptor-ligand interactions should be kept at the heart of scientific debate on infection. In this idea, the whole renin-angiotensin system has to be evaluated. We hypothesize that factors related to ethnicity, environment, behaviors, associated illness, and medications involving this complex system are probably responsible for situations regarded as anomalous from both an epidemiological and a clinical point of view, but, taken together, such factors may explain most of the aspects of current outbreak. We decided to use the analogy of a play and speculate about the possible impact in this tragedy of 1) air pollution via the interference of nitrogen dioxide on ACE2 expression; 2) the dual role of nicotine; 3) the hypothetical involvement of ACE2 polymorphisms, the relationships of which with ethnic factors and susceptibility to cardiovascular disease seems intriguing; 4) the impact on the severity of infection of hypertension and related medications acting on the renin/angiotensin system, and, finally, 5) the possible helpful role of chloroquine, thanks to its capacity of modifying ACE2 affinity to the viral spike protein by altering glycosylation. This hypothesis paper is an urgent call for the development of research programs that aim at questioning whether the putative protagonists of this tragedy are real-life actors in COVID-19.
DOI: 10.1016/j.biochi.2020.04.008
PubMed: 32305506
PubMed Central: PMC7161528
Affiliations:
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Electronic address: marco.alifano@aphp.fr.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Thoracic Surgery Department, Cochin Hospital, APHP Centre, University of Paris, France; INSERM U1138 Team «Cancer, Immune Control, and Escape», Cordeliers Research Center, University of Paris</wicri:regionArea><wicri:noRegion>University of Paris</wicri:noRegion><wicri:noRegion>University of Paris</wicri:noRegion></affiliation></author><author><name sortKey="Alifano, Pietro" sort="Alifano, Pietro" uniqKey="Alifano P" first="Pietro" last="Alifano">Pietro Alifano</name><affiliation wicri:level="1"><nlm:affiliation>Chair of Microbiology, Department of Biological and Environmental Sciences and Technologies, Salento University, Lecce, Italy.</nlm:affiliation><country xml:lang="fr">Italie</country><wicri:regionArea>Chair of Microbiology, Department of Biological and Environmental Sciences and Technologies, Salento University, Lecce</wicri:regionArea><wicri:noRegion>Lecce</wicri:noRegion></affiliation></author><author><name sortKey="Forgez, Patricia" sort="Forgez, Patricia" uniqKey="Forgez P" first="Patricia" last="Forgez">Patricia Forgez</name><affiliation wicri:level="3"><nlm:affiliation>Inserm UMR-S 1124 T3S, Eq 5 CELLULAR HOMEOSTASIS, CANCER and THERAPY, University of Paris, Campus Saint Germain, Paris, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Inserm UMR-S 1124 T3S, Eq 5 CELLULAR HOMEOSTASIS, CANCER and THERAPY, University of Paris, Campus Saint Germain, Paris</wicri:regionArea><placeName><region type="region">Île-de-France</region><region type="old region">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author><author><name sortKey="Iannelli, Antonio" sort="Iannelli, Antonio" uniqKey="Iannelli A" first="Antonio" last="Iannelli">Antonio Iannelli</name><affiliation wicri:level="1"><nlm:affiliation>Digestive Disease Department, Archet 2 Hospital, Nice University Hospital, University of Nice Côte d'Azur, Nice, France; 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Angiotensin converting enzyme 2 (ACE2), a component of the renin-angiotensin system, whose expression dominates on lung alveolar epithelial cells, is the human cell receptor of SARS-CoV-2, the causative agent of COVID-19. We strongly encourage the concept that thorough considerations of receptor-ligand interactions should be kept at the heart of scientific debate on infection. In this idea, the whole renin-angiotensin system has to be evaluated. We hypothesize that factors related to ethnicity, environment, behaviors, associated illness, and medications involving this complex system are probably responsible for situations regarded as anomalous from both an epidemiological and a clinical point of view, but, taken together, such factors may explain most of the aspects of current outbreak. We decided to use the analogy of a play and speculate about the possible impact in this tragedy of 1) air pollution via the interference of nitrogen dioxide on ACE2 expression; 2) the dual role of nicotine; 3) the hypothetical involvement of ACE2 polymorphisms, the relationships of which with ethnic factors and susceptibility to cardiovascular disease seems intriguing; 4) the impact on the severity of infection of hypertension and related medications acting on the renin/angiotensin system, and, finally, 5) the possible helpful role of chloroquine, thanks to its capacity of modifying ACE2 affinity to the viral spike protein by altering glycosylation. This hypothesis paper is an urgent call for the development of research programs that aim at questioning whether the putative protagonists of this tragedy are real-life actors in COVID-19.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">32305506</PMID><DateCompleted><Year>2020</Year><Month>06</Month><Day>11</Day></DateCompleted><DateRevised><Year>2020</Year><Month>06</Month><Day>11</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1638-6183</ISSN><JournalIssue CitedMedium="Internet"><Volume>174</Volume><PubDate><Year>2020</Year><Month>Jul</Month></PubDate></JournalIssue><Title>Biochimie</Title><ISOAbbreviation>Biochimie</ISOAbbreviation></Journal><ArticleTitle>Renin-angiotensin system at the heart of COVID-19 pandemic.</ArticleTitle><Pagination><MedlinePgn>30-33</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0300-9084(20)30078-X</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.biochi.2020.04.008</ELocationID><Abstract><AbstractText>Significant aspects of COVID-19 pandemic remain obscure. Angiotensin converting enzyme 2 (ACE2), a component of the renin-angiotensin system, whose expression dominates on lung alveolar epithelial cells, is the human cell receptor of SARS-CoV-2, the causative agent of COVID-19. We strongly encourage the concept that thorough considerations of receptor-ligand interactions should be kept at the heart of scientific debate on infection. In this idea, the whole renin-angiotensin system has to be evaluated. We hypothesize that factors related to ethnicity, environment, behaviors, associated illness, and medications involving this complex system are probably responsible for situations regarded as anomalous from both an epidemiological and a clinical point of view, but, taken together, such factors may explain most of the aspects of current outbreak. We decided to use the analogy of a play and speculate about the possible impact in this tragedy of 1) air pollution via the interference of nitrogen dioxide on ACE2 expression; 2) the dual role of nicotine; 3) the hypothetical involvement of ACE2 polymorphisms, the relationships of which with ethnic factors and susceptibility to cardiovascular disease seems intriguing; 4) the impact on the severity of infection of hypertension and related medications acting on the renin/angiotensin system, and, finally, 5) the possible helpful role of chloroquine, thanks to its capacity of modifying ACE2 affinity to the viral spike protein by altering glycosylation. This hypothesis paper is an urgent call for the development of research programs that aim at questioning whether the putative protagonists of this tragedy are real-life actors in COVID-19.</AbstractText><CopyrightInformation>Copyright © 2020 Elsevier B.V. and Société Française de Biochimie et Biologie Moléculaire (SFBBM). All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Alifano</LastName><ForeName>Marco</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Thoracic Surgery Department, Cochin Hospital, APHP Centre, University of Paris, France; INSERM U1138 Team «Cancer, Immune Control, and Escape», Cordeliers Research Center, University of Paris, France. Electronic address: marco.alifano@aphp.fr.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Alifano</LastName><ForeName>Pietro</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Chair of Microbiology, Department of Biological and Environmental Sciences and Technologies, Salento University, Lecce, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Forgez</LastName><ForeName>Patricia</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Inserm UMR-S 1124 T3S, Eq 5 CELLULAR HOMEOSTASIS, CANCER and THERAPY, University of Paris, Campus Saint Germain, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Iannelli</LastName><ForeName>Antonio</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Digestive Disease Department, Archet 2 Hospital, Nice University Hospital, University of Nice Côte d'Azur, Nice, France; Inserm, U1065, Team 8 "Hepatic Complications of Obesity", University Nice Côte d'Azur, France.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>04</Month><Day>16</Day></ArticleDate></Article><MedlineJournalInfo><Country>France</Country><MedlineTA>Biochimie</MedlineTA><NlmUniqueID>1264604</NlmUniqueID><ISSNLinking>0300-9084</ISSNLinking></MedlineJournalInfo><ChemicalList><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="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000073640" MajorTopicYN="N">Betacoronavirus</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002318" MajorTopicYN="N">Cardiovascular Diseases</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018352" MajorTopicYN="N">Coronavirus Infections</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006973" MajorTopicYN="N">Hypertension</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D058873" MajorTopicYN="N">Pandemics</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007703" MajorTopicYN="N">Peptidyl-Dipeptidase A</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011024" MajorTopicYN="N">Pneumonia, Viral</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012084" MajorTopicYN="N">Renin-Angiotensin System</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">ACE2</Keyword><Keyword MajorTopicYN="N">COVID-19</Keyword><Keyword MajorTopicYN="N">Mechanisms</Keyword></KeywordList><CoiStatement>Declaration of competing interest The authors have no conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2020</Year><Month>04</Month><Day>02</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2020</Year><Month>04</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2020</Year><Month>04</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>4</Month><Day>20</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>6</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>4</Month><Day>20</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32305506</ArticleId><ArticleId IdType="pii">S0300-9084(20)30078-X</ArticleId><ArticleId IdType="doi">10.1016/j.biochi.2020.04.008</ArticleId><ArticleId IdType="pmc">PMC7161528</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>France</li><li>Italie</li></country><region><li>Île-de-France</li></region><settlement><li>Paris</li></settlement></list><tree><country name="France"><noRegion><name sortKey="Alifano, Marco" sort="Alifano, Marco" uniqKey="Alifano M" first="Marco" last="Alifano">Marco Alifano</name></noRegion><name sortKey="Forgez, Patricia" sort="Forgez, Patricia" uniqKey="Forgez P" first="Patricia" last="Forgez">Patricia Forgez</name><name sortKey="Iannelli, Antonio" sort="Iannelli, Antonio" uniqKey="Iannelli A" first="Antonio" last="Iannelli">Antonio Iannelli</name></country><country name="Italie"><noRegion><name sortKey="Alifano, Pietro" sort="Alifano, Pietro" uniqKey="Alifano P" first="Pietro" last="Alifano">Pietro Alifano</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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