The role of epidermal growth factor receptor (EGFR) signaling in SARS coronavirus-induced pulmonary fibrosis
Identifieur interne : 000D49 ( Main/Exploration ); précédent : 000D48; suivant : 000D50The role of epidermal growth factor receptor (EGFR) signaling in SARS coronavirus-induced pulmonary fibrosis
Auteurs : Thiagarajan Venkataraman ; Matthew B. FriemanSource :
- Antiviral Research [ 0166-3542 ] ; 2017.
Descripteurs français
- KwdFr :
- Anatomopathologie moléculaire, Animaux, Cicatrisation de plaie (physiologie), Fibrose pulmonaire (anatomopathologie), Fibrose pulmonaire (métabolisme), Fibrose pulmonaire (virologie), Fibrose pulmonaire (étiologie), Humains, Interactions hôte-pathogène, Lésion pulmonaire (anatomopathologie), Lésion pulmonaire (virologie), Modèles animaux de maladie humaine, Récepteurs ErbB (métabolisme), Récepteurs ErbB (physiologie), Souris, Syndrome respiratoire aigu sévère (), Syndrome respiratoire aigu sévère (anatomopathologie), Syndrome respiratoire aigu sévère (métabolisme), Syndrome respiratoire aigu sévère (virologie), Transduction du signal (physiologie), Virus du SRAS (pathogénicité), Virus du SRAS (physiologie).
- MESH :
- anatomopathologie : Fibrose pulmonaire, Lésion pulmonaire, Syndrome respiratoire aigu sévère.
- métabolisme : Fibrose pulmonaire, Récepteurs ErbB, Syndrome respiratoire aigu sévère.
- pathogénicité : Virus du SRAS.
- physiologie : Cicatrisation de plaie, Récepteurs ErbB, Transduction du signal, Virus du SRAS.
- virologie : Fibrose pulmonaire, Lésion pulmonaire, Syndrome respiratoire aigu sévère.
- étiologie : Fibrose pulmonaire.
- Anatomopathologie moléculaire, Animaux, Humains, Interactions hôte-pathogène, Modèles animaux de maladie humaine, Souris, Syndrome respiratoire aigu sévère.
English descriptors
- KwdEn :
- Animals, Disease Models, Animal, ErbB Receptors (metabolism), ErbB Receptors (physiology), Host-Pathogen Interactions, Humans, Lung Injury (pathology), Lung Injury (virology), Mice, Pathology, Molecular, Pulmonary Fibrosis (etiology), Pulmonary Fibrosis (metabolism), Pulmonary Fibrosis (pathology), Pulmonary Fibrosis (virology), SARS Virus (pathogenicity), SARS Virus (physiology), Severe Acute Respiratory Syndrome (complications), Severe Acute Respiratory Syndrome (metabolism), Severe Acute Respiratory Syndrome (pathology), Severe Acute Respiratory Syndrome (virology), Signal Transduction (physiology), Wound Healing (physiology).
- MESH :
- chemical , metabolism : ErbB Receptors.
- chemical , physiology : ErbB Receptors.
- complications : Severe Acute Respiratory Syndrome.
- etiology : Pulmonary Fibrosis.
- metabolism : Pulmonary Fibrosis, Severe Acute Respiratory Syndrome.
- pathogenicity : SARS Virus.
- pathology : Lung Injury, Pulmonary Fibrosis, Severe Acute Respiratory Syndrome.
- physiology : SARS Virus, Signal Transduction, Wound Healing.
- virology : Lung Injury, Pulmonary Fibrosis, Severe Acute Respiratory Syndrome.
- Animals, Disease Models, Animal, Host-Pathogen Interactions, Humans, Mice, Pathology, Molecular.
Abstract
Many survivors of the 2003 outbreak of severe acute respiratory syndrome (SARS) developed residual pulmonary fibrosis with increased severity seen in older patients. Autopsies of patients that died from SARS also showed fibrosis to varying extents. Pulmonary fibrosis can be occasionally seen as a consequence to several respiratory viral infections but is much more common after a SARS coronavirus (SARS-CoV) infection. Given the threat of future outbreaks of severe coronavirus disease, including Middle East respiratory syndrome (MERS), it is important to understand the mechanisms responsible for pulmonary fibrosis, so as to support the development of therapeutic countermeasures and mitigate sequelae of infection. In this article, we summarize pulmonary fibrotic changes observed after a SARS-CoV infection, discuss the extent to which other respiratory viruses induce fibrosis, describe available animal models to study the development of SARS-CoV induced fibrosis and review evidence that pulmonary fibrosis is caused by a hyperactive host response to lung injury mediated by epidermal growth factor receptor (EGFR) signaling. We summarize work from our group and others indicating that inhibiting EGFR signaling may prevent an excessive fibrotic response to SARS-CoV and other respiratory viral infections and propose directions for future research.
Url:
DOI: 10.1016/j.antiviral.2017.03.022
PubMed: 28390872
PubMed Central: 5507769
Affiliations:
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Le document en format XML
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<term>Fibrose pulmonaire (métabolisme)</term>
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<term>Interactions hôte-pathogène</term>
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<front><div type="abstract" xml:lang="en"><p>Many survivors of the 2003 outbreak of severe acute respiratory syndrome (SARS) developed residual pulmonary fibrosis with increased severity seen in older patients. Autopsies of patients that died from SARS also showed fibrosis to varying extents. Pulmonary fibrosis can be occasionally seen as a consequence to several respiratory viral infections but is much more common after a SARS coronavirus (SARS-CoV) infection. Given the threat of future outbreaks of severe coronavirus disease, including Middle East respiratory syndrome (MERS), it is important to understand the mechanisms responsible for pulmonary fibrosis, so as to support the development of therapeutic countermeasures and mitigate sequelae of infection. In this article, we summarize pulmonary fibrotic changes observed after a SARS-CoV infection, discuss the extent to which other respiratory viruses induce fibrosis, describe available animal models to study the development of SARS-CoV induced fibrosis and review evidence that pulmonary fibrosis is caused by a hyperactive host response to lung injury mediated by epidermal growth factor receptor (EGFR) signaling. We summarize work from our group and others indicating that inhibiting EGFR signaling may prevent an excessive fibrotic response to SARS-CoV and other respiratory viral infections and propose directions for future research.</p>
</div>
</front>
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<tree><noCountry><name sortKey="Frieman, Matthew B" sort="Frieman, Matthew B" uniqKey="Frieman M" first="Matthew B." last="Frieman">Matthew B. Frieman</name>
<name sortKey="Venkataraman, Thiagarajan" sort="Venkataraman, Thiagarajan" uniqKey="Venkataraman T" first="Thiagarajan" last="Venkataraman">Thiagarajan Venkataraman</name>
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