Iron: Innocent bystander or vicious culprit in COVID-19 pathogenesis?
Identifieur interne : 000C36 ( Main/Exploration ); précédent : 000C35; suivant : 000C37Iron: Innocent bystander or vicious culprit in COVID-19 pathogenesis?
Auteurs : Marvin Edeas [France] ; Jumana Saleh [Oman] ; Carole Peyssonnaux [France]Source :
- International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases [ 1878-3511 ] ; 2020.
Descripteurs français
- KwdFr :
- Betacoronavirus (MeSH), Fer (sang), Hepcidines (physiologie), Humains (MeSH), Infections à coronavirus (anatomopathologie), Infections à coronavirus (mortalité), Inflammation (MeSH), Mitochondries (anatomopathologie), Mitochondries (physiologie), Pandémies (MeSH), Pneumopathie virale (anatomopathologie), Pneumopathie virale (mortalité), Stress oxydatif (MeSH), Surcharge en fer (virologie).
- MESH :
- anatomopathologie : Infections à coronavirus, Mitochondries, Pneumopathie virale.
- mortalité : Infections à coronavirus, Pneumopathie virale.
- physiologie : Hepcidines, Mitochondries.
- sang : Fer.
- virologie : Surcharge en fer.
- Betacoronavirus, Humains, Inflammation, Pandémies, Stress oxydatif.
English descriptors
- KwdEn :
- Betacoronavirus (MeSH), Coronavirus Infections (mortality), Coronavirus Infections (pathology), Cytokine Release Syndrome (virology), Ferroptosis (MeSH), Hepcidins (physiology), Humans (MeSH), Inflammation (MeSH), Iron (blood), Iron Overload (virology), Mitochondria (pathology), Mitochondria (physiology), Oxidative Stress (MeSH), Pandemics (MeSH), Pneumonia, Viral (mortality), Pneumonia, Viral (pathology).
- MESH :
- chemical , blood : Iron.
- chemical , physiology : Hepcidins.
- mortality : Coronavirus Infections, Pneumonia, Viral.
- pathology : Coronavirus Infections, Mitochondria, Pneumonia, Viral.
- physiology : Mitochondria.
- virology : Cytokine Release Syndrome, Iron Overload.
- Betacoronavirus, Ferroptosis, Humans, Inflammation, Oxidative Stress, Pandemics.
Abstract
The coronavirus 2 (SARS-CoV-2) pandemic is viciously spreading through the continents with rapidly increasing mortality rates. Current management of COVID-19 is based on the premise that respiratory failure is the leading cause of mortality. However, mounting evidence links accelerated pathogenesis in gravely ill COVID-19 patients to a hyper-inflammatory state involving a cytokine storm. Several components of the heightened inflammatory state were addressed as therapeutic targets. Another key component of the heightened inflammatory state is hyper-ferritinemia which reportedly identifies patients with increased mortality risk. In spite of its strong association with mortality, it is not yet clear if hyper-ferritinemia in COVID-19 patients is merely a systemic marker of disease progression, or a key modulator in disease pathogenesis. Here we address implications of a possible role for hyper-ferritinemia, and altered iron homeostasis in COVID-19 pathogenesis, and potential therapeutic targets in this regard.
DOI: 10.1016/j.ijid.2020.05.110
PubMed: 32497811
PubMed Central: PMC7264936
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Current management of COVID-19 is based on the premise that respiratory failure is the leading cause of mortality. However, mounting evidence links accelerated pathogenesis in gravely ill COVID-19 patients to a hyper-inflammatory state involving a cytokine storm. Several components of the heightened inflammatory state were addressed as therapeutic targets. Another key component of the heightened inflammatory state is hyper-ferritinemia which reportedly identifies patients with increased mortality risk. In spite of its strong association with mortality, it is not yet clear if hyper-ferritinemia in COVID-19 patients is merely a systemic marker of disease progression, or a key modulator in disease pathogenesis. Here we address implications of a possible role for hyper-ferritinemia, and altered iron homeostasis in COVID-19 pathogenesis, and potential therapeutic targets in this regard.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" IndexingMethod="Curated" Owner="NLM"><PMID Version="1">32497811</PMID><DateCompleted><Year>2020</Year><Month>07</Month><Day>30</Day></DateCompleted><DateRevised><Year>2020</Year><Month>09</Month><Day>09</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1878-3511</ISSN><JournalIssue CitedMedium="Internet"><Volume>97</Volume><PubDate><Year>2020</Year><Month>Aug</Month></PubDate></JournalIssue><Title>International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases</Title><ISOAbbreviation>Int. J. Infect. Dis.</ISOAbbreviation></Journal><ArticleTitle>Iron: Innocent bystander or vicious culprit in COVID-19 pathogenesis?</ArticleTitle><Pagination><MedlinePgn>303-305</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S1201-9712(20)30417-3</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.ijid.2020.05.110</ELocationID><Abstract><AbstractText>The coronavirus 2 (SARS-CoV-2) pandemic is viciously spreading through the continents with rapidly increasing mortality rates. Current management of COVID-19 is based on the premise that respiratory failure is the leading cause of mortality. However, mounting evidence links accelerated pathogenesis in gravely ill COVID-19 patients to a hyper-inflammatory state involving a cytokine storm. Several components of the heightened inflammatory state were addressed as therapeutic targets. Another key component of the heightened inflammatory state is hyper-ferritinemia which reportedly identifies patients with increased mortality risk. In spite of its strong association with mortality, it is not yet clear if hyper-ferritinemia in COVID-19 patients is merely a systemic marker of disease progression, or a key modulator in disease pathogenesis. Here we address implications of a possible role for hyper-ferritinemia, and altered iron homeostasis in COVID-19 pathogenesis, and potential therapeutic targets in this regard.</AbstractText><CopyrightInformation>Copyright © 2020 The Author(s). Published by Elsevier Ltd.. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Edeas</LastName><ForeName>Marvin</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Université de Paris, INSERM U1016, Institut Cochin, CNRS UMR8104, Paris, France; Laboratory of Excellence GR-Ex, Paris, France. Electronic address: marvin.edeas@inserm.fr.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Saleh</LastName><ForeName>Jumana</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>College of Medicine, Sultan Qaboos University, Oman.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Peyssonnaux</LastName><ForeName>Carole</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Université de Paris, INSERM U1016, Institut Cochin, CNRS UMR8104, Paris, France; Laboratory of Excellence GR-Ex, Paris, France.</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>06</Month><Day>02</Day></ArticleDate></Article><MedlineJournalInfo><Country>Canada</Country><MedlineTA>Int J Infect 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MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000080424" MajorTopicYN="N">Cytokine Release Syndrome</DescriptorName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000079403" MajorTopicYN="N">Ferroptosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D064451" MajorTopicYN="N">Hepcidins</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007249" MajorTopicYN="N">Inflammation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007501" MajorTopicYN="N">Iron</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019190" MajorTopicYN="N">Iron Overload</DescriptorName><QualifierName UI="Q000821" MajorTopicYN="Y">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008928" MajorTopicYN="N">Mitochondria</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018384" MajorTopicYN="N">Oxidative Stress</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D058873" MajorTopicYN="N">Pandemics</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011024" MajorTopicYN="N">Pneumonia, Viral</DescriptorName><QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Ferroptosis</Keyword><Keyword MajorTopicYN="N">Hyper-ferritinemia</Keyword><Keyword MajorTopicYN="N">Hypercoagulability</Keyword><Keyword MajorTopicYN="N">Iron 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