Autophagy as an emerging target for COVID-19: lessons from an old friend, chloroquine.
Identifieur interne : 001439 ( Main/Curation ); précédent : 001438; suivant : 001440Autophagy as an emerging target for COVID-19: lessons from an old friend, chloroquine.
Auteurs : Srinivasa Reddy Bonam [France] ; Sylviane Muller [France] ; Jagadeesh Bayry [France] ; Daniel J. Klionsky [États-Unis]Source :
- Autophagy [ 1554-8635 ] ; 2020.
Descripteurs français
- KwdFr :
- Autophagie (effets des médicaments et des substances chimiques), Autophagie (physiologie), Chloroquine (pharmacologie), Chloroquine (usage thérapeutique), Concentration en ions d'hydrogène (effets des médicaments et des substances chimiques), Endosomes (effets des médicaments et des substances chimiques), Endosomes (métabolisme), Humains (MeSH), Hydroxychloroquine (pharmacologie), Hydroxychloroquine (usage thérapeutique), Immunité innée (physiologie), Indice de gravité de la maladie (MeSH), Lysosomes (effets des médicaments et des substances chimiques), Lysosomes (métabolisme), Thérapie moléculaire ciblée (méthodes), Thérapie moléculaire ciblée (tendances).
- MESH :
- effets des médicaments et des substances chimiques : Autophagie, Concentration en ions d'hydrogène, Endosomes, Lysosomes.
- métabolisme : Endosomes, Lysosomes.
- méthodes : Thérapie moléculaire ciblée.
- pharmacologie : Chloroquine, Hydroxychloroquine.
- physiologie : Autophagie, Immunité innée.
- tendances : Thérapie moléculaire ciblée.
- usage thérapeutique : Chloroquine, Hydroxychloroquine.
- Humains, Indice de gravité de la maladie.
English descriptors
- KwdEn :
- Autophagy (drug effects), Autophagy (physiology), COVID-19 (drug therapy), COVID-19 (immunology), COVID-19 (pathology), COVID-19 (virology), Chloroquine (pharmacology), Chloroquine (therapeutic use), Endosomes (drug effects), Endosomes (metabolism), Humans (MeSH), Hydrogen-Ion Concentration (drug effects), Hydroxychloroquine (pharmacology), Hydroxychloroquine (therapeutic use), Immunity, Innate (physiology), Lysosomes (drug effects), Lysosomes (metabolism), Molecular Targeted Therapy (methods), Molecular Targeted Therapy (trends), SARS-CoV-2 (drug effects), SARS-CoV-2 (immunology), SARS-CoV-2 (pathogenicity), Severity of Illness Index (MeSH).
- MESH :
- chemical , pharmacology : Chloroquine, Hydroxychloroquine.
- drug effects : Autophagy, Endosomes, Hydrogen-Ion Concentration, Lysosomes, SARS-CoV-2.
- drug therapy : COVID-19.
- immunology : COVID-19, SARS-CoV-2.
- metabolism : Endosomes, Lysosomes.
- methods : Molecular Targeted Therapy.
- pathogenicity : SARS-CoV-2.
- pathology : COVID-19.
- physiology : Autophagy, Immunity, Innate.
- chemical , therapeutic use : Chloroquine, Hydroxychloroquine.
- trends : Molecular Targeted Therapy.
- virology : COVID-19.
- Humans, Severity of Illness Index.
Abstract
During the last week of December 2019, Wuhan (China) was confronted with the first case of respiratory tract disease 2019 (coronavirus disease 2019, COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Due to the rapid outbreak of the transmission (~3.64 million positive cases and high mortality as of 5 May 2020), the world is looking for immediate and better therapeutic options. Still, much information is not known, including origin of the disease, complete genomic characterization, mechanism of transmission dynamics, extent of spread, possible genetic predisposition, clinical and biological diagnosis, complete details of disease-induced pathogenicity, and possible therapeutic options. Although several known drugs are already under clinical evaluation with many in repositioning strategies, much attention has been paid to the aminoquinoline derivates, chloroquine (CQ) and hydroxychloroquine (HCQ). These molecules are known regulators of endosomes/lysosomes, which are subcellular organelles central to autophagy processes. By elevating the pH of acidic endosomes/lysosomes, CQ/HCQ inhibit the autophagic process. In this short perspective, we discuss the roles of CQ/HCQ in the treatment of COVID-19 patients and propose new ways of possible treatment for SARS-CoV-2 infection based on the molecules that selectivity target autophagy.Abbreviation: ACE2: angiotensin I converting enzyme 2; CoV: coronavirus; CQ: chloroquine; ER: endoplasmic reticulum; HCQ: hydroxychloroquine; MERS-CoV: Middle East respiratory syndrome coronavirus; SARS-CoV: severe acute respiratory syndrome coronavirus; SARS-CoV-2: severe acute respiratory syndrome coronavirus 2.
DOI: 10.1080/15548627.2020.1779467
PubMed: 32522067
PubMed Central: PMC7755324
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pubmed:32522067Le document en format XML
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<front><div type="abstract" xml:lang="en">During the last week of December 2019, Wuhan (China) was confronted with the first case of respiratory tract disease 2019 (coronavirus disease 2019, COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Due to the rapid outbreak of the transmission (~3.64 million positive cases and high mortality as of 5 May 2020), the world is looking for immediate and better therapeutic options. Still, much information is not known, including origin of the disease, complete genomic characterization, mechanism of transmission dynamics, extent of spread, possible genetic predisposition, clinical and biological diagnosis, complete details of disease-induced pathogenicity, and possible therapeutic options. Although several known drugs are already under clinical evaluation with many in repositioning strategies, much attention has been paid to the aminoquinoline derivates, chloroquine (CQ) and hydroxychloroquine (HCQ). These molecules are known regulators of endosomes/lysosomes, which are subcellular organelles central to autophagy processes. By elevating the pH of acidic endosomes/lysosomes, CQ/HCQ inhibit the autophagic process. In this short perspective, we discuss the roles of CQ/HCQ in the treatment of COVID-19 patients and propose new ways of possible treatment for SARS-CoV-2 infection based on the molecules that selectivity target autophagy.<b>Abbreviation:</b>
ACE2: angiotensin I converting enzyme 2; CoV: coronavirus; CQ: chloroquine; ER: endoplasmic reticulum; HCQ: hydroxychloroquine; MERS-CoV: Middle East respiratory syndrome coronavirus; SARS-CoV: severe acute respiratory syndrome coronavirus; SARS-CoV-2: severe acute respiratory syndrome coronavirus 2.</div>
</front>
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<DateCompleted><Year>2020</Year>
<Month>12</Month>
<Day>30</Day>
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<DateRevised><Year>2021</Year>
<Month>04</Month>
<Day>22</Day>
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<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1554-8635</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>16</Volume>
<Issue>12</Issue>
<PubDate><Year>2020</Year>
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<Title>Autophagy</Title>
<ISOAbbreviation>Autophagy</ISOAbbreviation>
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<ArticleTitle>Autophagy as an emerging target for COVID-19: lessons from an old friend, chloroquine.</ArticleTitle>
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<Abstract><AbstractText>During the last week of December 2019, Wuhan (China) was confronted with the first case of respiratory tract disease 2019 (coronavirus disease 2019, COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Due to the rapid outbreak of the transmission (~3.64 million positive cases and high mortality as of 5 May 2020), the world is looking for immediate and better therapeutic options. Still, much information is not known, including origin of the disease, complete genomic characterization, mechanism of transmission dynamics, extent of spread, possible genetic predisposition, clinical and biological diagnosis, complete details of disease-induced pathogenicity, and possible therapeutic options. Although several known drugs are already under clinical evaluation with many in repositioning strategies, much attention has been paid to the aminoquinoline derivates, chloroquine (CQ) and hydroxychloroquine (HCQ). These molecules are known regulators of endosomes/lysosomes, which are subcellular organelles central to autophagy processes. By elevating the pH of acidic endosomes/lysosomes, CQ/HCQ inhibit the autophagic process. In this short perspective, we discuss the roles of CQ/HCQ in the treatment of COVID-19 patients and propose new ways of possible treatment for SARS-CoV-2 infection based on the molecules that selectivity target autophagy.<b>Abbreviation:</b>
ACE2: angiotensin I converting enzyme 2; CoV: coronavirus; CQ: chloroquine; ER: endoplasmic reticulum; HCQ: hydroxychloroquine; MERS-CoV: Middle East respiratory syndrome coronavirus; SARS-CoV: severe acute respiratory syndrome coronavirus; SARS-CoV-2: severe acute respiratory syndrome coronavirus 2.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Bonam</LastName>
<ForeName>Srinivasa Reddy</ForeName>
<Initials>SR</Initials>
<Identifier Source="ORCID">0000-0002-2888-2418</Identifier>
<AffiliationInfo><Affiliation>Institut National de la Santé et de la Recherche Médicale; Centre de Recherche des Cordeliers, Equipe- Immunopathologie et Immunointervention Thérapeutique, Sorbonne Université, Université De Paris , Paris, France.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Muller</LastName>
<ForeName>Sylviane</ForeName>
<Initials>S</Initials>
<Identifier Source="ORCID">0000-0002-0481-0620</Identifier>
<AffiliationInfo><Affiliation>CNRS and Strasbourg University Unit Biotechnology and Cell signalling / Laboratory of excellence Medalis , Strasbourg, France.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Fédération Hospitalo-Universitaire OMICARE, Fédération de Médecine Translationnelle de Strasbourg (FMTS), Strasbourg University , Strasbourg, France.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Chair of Therapeutic Immunology, University of Strasbourg Institute for Advanced Study (USIAS) , Strasbourg, France.</Affiliation>
</AffiliationInfo>
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<ForeName>Jagadeesh</ForeName>
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<AffiliationInfo><Affiliation>Institut National de la Santé et de la Recherche Médicale; Centre de Recherche des Cordeliers, Equipe- Immunopathologie et Immunointervention Thérapeutique, Sorbonne Université, Université De Paris , Paris, France.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Klionsky</LastName>
<ForeName>Daniel J</ForeName>
<Initials>DJ</Initials>
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<AffiliationInfo><Affiliation>Life Sciences Institute and Department of Molecular, Cellular and Developmental Biology, University of Michigan , Ann Arbor, MI, USA.</Affiliation>
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<NameOfSubstance UI="D006886">Hydroxychloroquine</NameOfSubstance>
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