COVID-19 in the heart and the lungs: could we “Notch” the inflammatory storm?
Identifieur interne : 000923 ( Main/Exploration ); précédent : 000922; suivant : 000924COVID-19 in the heart and the lungs: could we “Notch” the inflammatory storm?
Auteurs : Paola Rizzo [Italie] ; Francesco Vieceli Dalla Sega [Italie] ; Francesca Fortini [Italie] ; Luisa Marracino [Italie] ; Claudio Rapezzi [Italie] ; Roberto Ferrari [Italie]Source :
- Basic Research in Cardiology [ 0300-8428 ] ; 2020.
Descripteurs français
- KwdFr :
- Arrêt cardiaque (anatomopathologie), Arrêt cardiaque (étiologie), Cardiopathies (anatomopathologie), Cardiopathies (physiopathologie), Cardiopathies (traitement médicamenteux), Cardiopathies (étiologie), Chine, Défaillance cardiaque (anatomopathologie), Défaillance cardiaque (étiologie), Furine (métabolisme), Humains, Infections à coronavirus (anatomopathologie), Infections à coronavirus (physiopathologie), Infections à coronavirus (traitement médicamenteux), Infections à coronavirus (virologie), Interleukine-6 (immunologie), Maladies pulmonaires (anatomopathologie), Maladies pulmonaires (physiopathologie), Maladies pulmonaires (traitement médicamenteux), Maladies pulmonaires (étiologie), Myocardite (anatomopathologie), Myocardite (étiologie), Pandémies, Peptidyl-Dipeptidase A (déficit), Peptidyl-Dipeptidase A (métabolisme), Pneumopathie virale (anatomopathologie), Pneumopathie virale (physiopathologie), Pneumopathie virale (traitement médicamenteux), Pneumopathie virale (virologie), Protéine ADAM17 (antagonistes et inhibiteurs), Récepteurs Notch (antagonistes et inhibiteurs), Récepteurs Notch (métabolisme), Transduction du signal (), Évolution de la maladie.
- MESH :
- anatomopathologie : Arrêt cardiaque, Cardiopathies, Défaillance cardiaque, Infections à coronavirus, Maladies pulmonaires, Myocardite, Pneumopathie virale.
- antagonistes et inhibiteurs : Protéine ADAM17, Récepteurs Notch.
- déficit : Peptidyl-Dipeptidase A.
- immunologie : Interleukine-6.
- métabolisme : Furine, Peptidyl-Dipeptidase A, Récepteurs Notch.
- physiopathologie : Cardiopathies, Infections à coronavirus, Maladies pulmonaires, Pneumopathie virale.
- traitement médicamenteux : Cardiopathies, Infections à coronavirus, Maladies pulmonaires, Pneumopathie virale.
- virologie : Infections à coronavirus, Pneumopathie virale.
- étiologie : Arrêt cardiaque, Cardiopathies, Défaillance cardiaque, Maladies pulmonaires, Myocardite.
- Chine, Humains, Pandémies, Transduction du signal, Évolution de la maladie.
- Wicri :
- geographic : République populaire de Chine.
English descriptors
- KwdEn :
- ADAM17 Protein (antagonists & inhibitors), Betacoronavirus (drug effects), Betacoronavirus (pathogenicity), China, Coronavirus Infections (drug therapy), Coronavirus Infections (pathology), Coronavirus Infections (physiopathology), Coronavirus Infections (virology), Disease Progression, Furin (metabolism), Heart Arrest (etiology), Heart Arrest (pathology), Heart Diseases (drug therapy), Heart Diseases (etiology), Heart Diseases (pathology), Heart Diseases (physiopathology), Heart Failure (etiology), Heart Failure (pathology), Humans, Interleukin-6 (immunology), Lung Diseases (drug therapy), Lung Diseases (etiology), Lung Diseases (pathology), Lung Diseases (physiopathology), Myocarditis (etiology), Myocarditis (pathology), Pandemics, Peptidyl-Dipeptidase A (deficiency), Peptidyl-Dipeptidase A (metabolism), Pneumonia, Viral (drug therapy), Pneumonia, Viral (pathology), Pneumonia, Viral (physiopathology), Pneumonia, Viral (virology), Receptors, Notch (antagonists & inhibitors), Receptors, Notch (metabolism), Signal Transduction (drug effects).
- MESH :
- chemical , antagonists & inhibitors : ADAM17 Protein, Receptors, Notch.
- chemical , deficiency : Peptidyl-Dipeptidase A.
- chemical , immunology : Interleukin-6.
- chemical , metabolism : Furin, Peptidyl-Dipeptidase A, Receptors, Notch.
- geographic : China.
- drug effects : Betacoronavirus, Signal Transduction.
- drug therapy : Coronavirus Infections, Heart Diseases, Lung Diseases, Pneumonia, Viral.
- etiology : Heart Arrest, Heart Diseases, Heart Failure, Lung Diseases, Myocarditis.
- pathogenicity : Betacoronavirus.
- pathology : Coronavirus Infections, Heart Arrest, Heart Diseases, Heart Failure, Lung Diseases, Myocarditis, Pneumonia, Viral.
- physiopathology : Coronavirus Infections, Heart Diseases, Lung Diseases, Pneumonia, Viral.
- virology : Coronavirus Infections, Pneumonia, Viral.
- Disease Progression, Humans, Pandemics.
Abstract
From January 2020, coronavirus disease (COVID-19) originated in China has spread around the world. The disease is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The presence of myocarditis, cardiac arrest, and acute heart failure in COVID-19 patients suggests the existence of a relationship between SARS-CoV-2 infection and cardiac disease. The Notch signalling is a major regulator of cardiovascular function and it is also implicated in several biological processes mediating viral infections. In this report we discuss the possibility to target Notch signalling to prevent SARS-CoV-2 infection and interfere with the progression of COVID-19- associated heart and lungs disease.
Url:
DOI: 10.1007/s00395-020-0791-5
PubMed: 32274570
PubMed Central: 7144545
Affiliations:
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Cona,</institution></institution-wrap>Ferrara, Italy</nlm:aff><country xml:lang="fr">Italie</country><wicri:regionArea>Ferrara</wicri:regionArea></affiliation></author></analytic><series><title level="j">Basic Research in Cardiology</title><idno type="ISSN">0300-8428</idno><idno type="eISSN">1435-1803</idno><imprint><date when="2020">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>ADAM17 Protein (antagonists & inhibitors)</term><term>Betacoronavirus (drug effects)</term><term>Betacoronavirus (pathogenicity)</term><term>China</term><term>Coronavirus Infections (drug therapy)</term><term>Coronavirus Infections (pathology)</term><term>Coronavirus Infections (physiopathology)</term><term>Coronavirus Infections (virology)</term><term>Disease Progression</term><term>Furin (metabolism)</term><term>Heart Arrest (etiology)</term><term>Heart Arrest (pathology)</term><term>Heart Diseases (drug therapy)</term><term>Heart Diseases (etiology)</term><term>Heart Diseases (pathology)</term><term>Heart Diseases (physiopathology)</term><term>Heart Failure (etiology)</term><term>Heart Failure (pathology)</term><term>Humans</term><term>Interleukin-6 (immunology)</term><term>Lung Diseases (drug therapy)</term><term>Lung Diseases (etiology)</term><term>Lung Diseases (pathology)</term><term>Lung Diseases (physiopathology)</term><term>Myocarditis (etiology)</term><term>Myocarditis (pathology)</term><term>Pandemics</term><term>Peptidyl-Dipeptidase A (deficiency)</term><term>Peptidyl-Dipeptidase A (metabolism)</term><term>Pneumonia, Viral (drug therapy)</term><term>Pneumonia, Viral (pathology)</term><term>Pneumonia, Viral (physiopathology)</term><term>Pneumonia, Viral (virology)</term><term>Receptors, Notch (antagonists & inhibitors)</term><term>Receptors, Notch (metabolism)</term><term>Signal Transduction (drug effects)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Arrêt cardiaque (anatomopathologie)</term><term>Arrêt cardiaque (étiologie)</term><term>Cardiopathies (anatomopathologie)</term><term>Cardiopathies (physiopathologie)</term><term>Cardiopathies (traitement médicamenteux)</term><term>Cardiopathies (étiologie)</term><term>Chine</term><term>Défaillance cardiaque (anatomopathologie)</term><term>Défaillance cardiaque (étiologie)</term><term>Furine (métabolisme)</term><term>Humains</term><term>Infections à coronavirus (anatomopathologie)</term><term>Infections à coronavirus (physiopathologie)</term><term>Infections à coronavirus (traitement médicamenteux)</term><term>Infections à coronavirus (virologie)</term><term>Interleukine-6 (immunologie)</term><term>Maladies pulmonaires (anatomopathologie)</term><term>Maladies pulmonaires (physiopathologie)</term><term>Maladies pulmonaires (traitement médicamenteux)</term><term>Maladies pulmonaires (étiologie)</term><term>Myocardite (anatomopathologie)</term><term>Myocardite (étiologie)</term><term>Pandémies</term><term>Peptidyl-Dipeptidase A (déficit)</term><term>Peptidyl-Dipeptidase A (métabolisme)</term><term>Pneumopathie virale (anatomopathologie)</term><term>Pneumopathie virale (physiopathologie)</term><term>Pneumopathie virale (traitement médicamenteux)</term><term>Pneumopathie virale (virologie)</term><term>Protéine ADAM17 (antagonistes et inhibiteurs)</term><term>Récepteurs Notch (antagonistes et inhibiteurs)</term><term>Récepteurs Notch (métabolisme)</term><term>Transduction du signal ()</term><term>Évolution de la maladie</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>ADAM17 Protein</term><term>Receptors, Notch</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Peptidyl-Dipeptidase A</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Interleukin-6</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Furin</term><term>Peptidyl-Dipeptidase A</term><term>Receptors, Notch</term></keywords><keywords scheme="MESH" type="geographic" xml:lang="en"><term>China</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Arrêt cardiaque</term><term>Cardiopathies</term><term>Défaillance cardiaque</term><term>Infections à coronavirus</term><term>Maladies pulmonaires</term><term>Myocardite</term><term>Pneumopathie virale</term></keywords><keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Protéine ADAM17</term><term>Récepteurs Notch</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Betacoronavirus</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Coronavirus Infections</term><term>Heart Diseases</term><term>Lung Diseases</term><term>Pneumonia, Viral</term></keywords><keywords scheme="MESH" qualifier="déficit" xml:lang="fr"><term>Peptidyl-Dipeptidase A</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Heart Arrest</term><term>Heart Diseases</term><term>Heart Failure</term><term>Lung Diseases</term><term>Myocarditis</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Interleukine-6</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Furine</term><term>Peptidyl-Dipeptidase A</term><term>Récepteurs Notch</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Betacoronavirus</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Coronavirus Infections</term><term>Heart Arrest</term><term>Heart Diseases</term><term>Heart Failure</term><term>Lung Diseases</term><term>Myocarditis</term><term>Pneumonia, Viral</term></keywords><keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Cardiopathies</term><term>Infections à coronavirus</term><term>Maladies pulmonaires</term><term>Pneumopathie virale</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Coronavirus Infections</term><term>Heart Diseases</term><term>Lung Diseases</term><term>Pneumonia, Viral</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Cardiopathies</term><term>Infections à coronavirus</term><term>Maladies pulmonaires</term><term>Pneumopathie virale</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" qualifier="étiologie" xml:lang="fr"><term>Arrêt cardiaque</term><term>Cardiopathies</term><term>Défaillance cardiaque</term><term>Maladies pulmonaires</term><term>Myocardite</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Disease Progression</term><term>Humans</term><term>Pandemics</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Chine</term><term>Humains</term><term>Pandémies</term><term>Transduction du signal</term><term>Évolution de la maladie</term></keywords><keywords scheme="Wicri" type="geographic" xml:lang="fr"><term>République populaire de Chine</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="Par1">From January 2020, coronavirus disease (COVID-19) originated in China has spread around the world. The disease is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The presence of myocarditis, cardiac arrest, and acute heart failure in COVID-19 patients suggests the existence of a relationship between SARS-CoV-2 infection and cardiac disease. The Notch signalling is a major regulator of cardiovascular function and it is also implicated in several biological processes mediating viral infections. In this report we discuss the possibility to target Notch signalling to prevent SARS-CoV-2 infection and interfere with the progression of COVID-19- associated heart and lungs disease.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Agata, J" uniqKey="Agata J">J Agata</name></author><author><name sortKey="Ura, N" uniqKey="Ura N">N Ura</name></author><author><name sortKey="Yoshida, H" uniqKey="Yoshida H">H Yoshida</name></author><author><name sortKey="Shinshi, Y" uniqKey="Shinshi Y">Y Shinshi</name></author><author><name sortKey="Sasaki, H" uniqKey="Sasaki H">H Sasaki</name></author><author><name sortKey="Hyakkoku, M" uniqKey="Hyakkoku M">M Hyakkoku</name></author><author><name sortKey="Taniguchi, S" uniqKey="Taniguchi S">S Taniguchi</name></author><author><name sortKey="Shimamoto, K" uniqKey="Shimamoto K">K Shimamoto</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Aquila, G" uniqKey="Aquila G">G 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sortKey="Zhan, F" uniqKey="Zhan F">F Zhan</name></author><author><name sortKey="Ma, X" uniqKey="Ma X">X Ma</name></author><author><name sortKey="Wang, D" uniqKey="Wang D">D Wang</name></author><author><name sortKey="Xu, W" uniqKey="Xu W">W Xu</name></author><author><name sortKey="Wu, G" uniqKey="Wu G">G Wu</name></author><author><name sortKey="Gao, Gf" uniqKey="Gao G">GF Gao</name></author><author><name sortKey="Tan, W" uniqKey="Tan W">W Tan</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>Italie</li></country></list><tree><country name="Italie"><noRegion><name sortKey="Rizzo, Paola" sort="Rizzo, Paola" uniqKey="Rizzo P" first="Paola" last="Rizzo">Paola Rizzo</name></noRegion><name sortKey="Ferrari, Roberto" sort="Ferrari, Roberto" uniqKey="Ferrari R" first="Roberto" last="Ferrari">Roberto Ferrari</name><name sortKey="Ferrari, Roberto" sort="Ferrari, Roberto" uniqKey="Ferrari R" first="Roberto" last="Ferrari">Roberto Ferrari</name><name sortKey="Fortini, Francesca" sort="Fortini, Francesca" uniqKey="Fortini F" first="Francesca" last="Fortini">Francesca Fortini</name><name sortKey="Marracino, Luisa" sort="Marracino, Luisa" uniqKey="Marracino L" first="Luisa" last="Marracino">Luisa Marracino</name><name sortKey="Rapezzi, Claudio" sort="Rapezzi, Claudio" uniqKey="Rapezzi C" first="Claudio" last="Rapezzi">Claudio Rapezzi</name><name sortKey="Rapezzi, Claudio" sort="Rapezzi, Claudio" uniqKey="Rapezzi C" first="Claudio" last="Rapezzi">Claudio Rapezzi</name><name sortKey="Rizzo, Paola" sort="Rizzo, Paola" uniqKey="Rizzo P" first="Paola" last="Rizzo">Paola Rizzo</name><name sortKey="Vieceli Dalla Sega, Francesco" sort="Vieceli Dalla Sega, Francesco" uniqKey="Vieceli Dalla Sega F" first="Francesco" last="Vieceli Dalla Sega">Francesco Vieceli Dalla Sega</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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