ArticleJournal of virology2017
Overactive Epidermal Growth Factor Receptor Signaling Leads to Increased Fibrosis after Severe Acute Respiratory Syndrome Coronavirus Infection.
Article in Journal of virology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
72 citing papers in PubMed, 114 citations in OpenAlex.
- Epigenetic and microRNA-mediated regulation of pulmonary fibrosis and immune dysregulation in fatal COVID-19.Molecular medicine (Cambridge, Mass.) · 2026Article
- Peripheral blood cytokines during early and post-acute stages of SARS-CoV-2 infection are associated with disease severity and long-term symptoms.Frontiers in immunology · 2026Article
- Airway epithelial SARS-CoV-2 infectious and repair responses: relationships to age, sex, and post-COVID pulmonary syndromes.bioRxiv : the preprint server for biology · 2025Article
- Transcriptional repressor Capicua is a gatekeeper of cell-intrinsic interferon responses.Cell host & microbe · 2025Article
- Neurobiology of COVID-19-Associated Psychosis/Schizophrenia: Implication of Epidermal Growth Factor Receptor Signaling.Neuropsychopharmacology reports · 2025Review
- Fuzheng Huayu tablets for treating pulmonary fibrosis in post-COVID-19 patients: a multicenter, randomized, double-blind, placebo-controlled trial.Frontiers in pharmacology · 2025Article
- Mechanistic insights into traditional Chinese medicine for viral pneumonia treatment: signaling pathway perspectives.Frontiers in pharmacology · 2025Review
- Outcome of SARS-CoV-2 reinfection depends on genetic background in female mice.Nature communications · 2024Article
- SARS-CoV-2 aberrantly elevates mitochondrial bioenergetics to induce robust virus propagation.Signal transduction and targeted therapy · 2024Article
- Human iPSC-Based Model of COPD to Investigate Disease Mechanisms, Predict SARS-COV-2 Outcome, and Test Preventive Immunotherapy.Stem cells (Dayton, Ohio) · 2024Article
- HB-EGF Plasmatic Level Contributes to the Development of Early Risk Prediction Nomogram for Severe COVID-19 Cases.Biomedicines · 2024Article
- Antifibrotic Drugs against Idiopathic Pulmonary Fibrosis and Pulmonary Fibrosis Induced by COVID-19: Therapeutic Approaches and Potential Diagnostic Biomarkers.International journal of molecular sciences · 2024Review
- Article
- Clinical outcomes and immunological response to SARS-CoV-2 infection among people living with HIV.Experimental biology and medicine (Maywood, N.J.) · 2024Review
- Role of Virus-Induced EGFR Trafficking in Proviral Functions.Biomolecules · 2023Review
- Host immune responses associated with SARS-CoV-2 Omicron infection result in protection or pathology during reinfection depending on mouse genetic background.Research square · 2023Article
- Anticancer pan-ErbB inhibitors reduce inflammation and tissue injury and exert broad-spectrum antiviral effects.The Journal of clinical investigation · 2023Article
- Long-Term Radiological Pulmonary Changes in Mechanically Ventilated Patients with Respiratory Failure due to SARS-CoV-2 Infection.Biomedicines · 2023Article
- Repurposing clinically available drugs and therapies for pathogenic targets to combat SARS-CoV-2.MedComm · 2023Review
- Deciphering molecular mechanisms of SARS-CoV-2 pathogenesis and drug repurposing through GRN motifs: a comprehensive systems biology study.3 Biotech · 2023Article
12 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Severe acute respiratory syndrome coronavirus (SARS-CoV) is a highly pathogenic respiratory virus that causes morbidity and mortality in humans. After infection with SARS-CoV, the acute lung injury caused by the virus must be repaired to regain lung function. A dysregulation in this wound healing process leads to fibrosis. Many survivors of SARS-CoV infection develop pulmonary fibrosis (PF), with higher prevalence in older patients. Using mouse models of SARS-CoV pathogenesis, we have identified that the wound repair pathway, controlled by the epidermal growth factor receptor (EGFR), is critical to recovery from SARS-CoV-induced tissue damage. In mice with constitutively active EGFR [EGFR(DSK5) mice], we find that SARS-CoV infection causes enhanced lung disease. Importantly, we show that during infection, the EGFR ligands amphiregulin and heparin-binding EGF-like growth factor (HB-EGF) are upregulated, and exogenous addition of these ligands during infection leads to enhanced lung disease and altered wound healing dynamics. Our data demonstrate a key role of EGFR in the host response to SARS-CoV and how it may be implicated in lung disease induced by other highly pathogenic respiratory viruses.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.