ArticleOncotarget2015
The activation of EGFR promotes myocardial tumor necrosis factor-α production and cardiac failure in endotoxemia.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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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.
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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
13 citing papers in PubMed, 22 citations in OpenAlex.
- Whole transcriptome analysis and preliminary construction of ceRNA networks in obstetric antiphospholipid syndrome.Frontiers in immunology · 2025Article
- Emodin inhibits M1 macrophage activation that related to acute and chronic kidney injury through EGFR/MAPK pathway.Functional & integrative genomics · 2024Article
- EGFR promotes the apoptosis of CD4Journal of advanced research · 2023Article
- EGFR tyrosine kinase activity and Rab GTPases coordinate EGFR trafficking to regulate macrophage activation in sepsis.Cell death & disease · 2022Article
- Blockade of the P2Y2 Receptor Attenuates Alcoholic Liver Inflammation by Targeting the EGFR-ERK1/2 Signaling Pathway.Drug design, development and therapy · 2022Article
- Erlotinib protests against LPS-induced parthanatos through inhibiting macrophage surface TLR4 expression.Cell death discovery · 2021Article
- Targeting the eCIRP/TREM-1 interaction with a small molecule inhibitor improves cardiac dysfunction in neonatal sepsis.Molecular medicine (Cambridge, Mass.) · 2020Article
- New markers for sepsis caused by Pseudomonas aeruginosa during burn infection.Metabolomics : Official journal of the Metabolomic Society · 2020Article
- Autophagic flux is essential for the downregulation of D-dopachrome tautomerase by atractylenolide I to ameliorate intestinal adenoma formation.Journal of cell communication and signaling · 2018Article
- Mig6 reduces inflammatory mediators production by regulating the activation of EGFR in LPS-induced endotoxemia.Journal of cellular physiology · 2018Article
- Targeted Therapies: Immunologic Effects and Potential Applications Outside of Cancer.Journal of clinical pharmacology · 2018Review
- Exogenous carbon monoxide inhibits neutrophil infiltration in LPS-induced sepsis by interfering with FPR1 via p38 MAPK but not GRK2.Oncotarget · 2016Article
- A Disintegrin and Metalloprotease 17 in the Cardiovascular and Central Nervous Systems.Frontiers in physiology · 2016Review
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To study the effect of EGFR activation on the generation of TNF-α and the occurrence of cardiac dysfuncetion during sepsis, PD168393 and erlotinib (both are EGFR inhibitors) were applied to decreased the production of TNF-α and phosphrylation of ERK1/2 and p38 induced by LPS in cardiomyocytes. These results were further proved by specifically knocked down the expression of EGFR in vitro. Both TAPI-1, a TNF-α converting enzyme (TACE) inhibitor, and TGF-α neutralizing antibody could inhibit the activation of EGFR and the generation of TNF-α mRNA after LPS treatment. The increase of TGF-α in response to LPS could also be suppressed by TAPI-1. On the other hand, exogenous TGF-α increased the expression of TNF-α mRNA and partially reversed the inhibitory effect of TAPI-1 on expression of TNF-α mRNA in response to LPS indicating that the transactivation of EGFR by LPS in cardiomyocytes needs the help of TACE and TGF-α. In endotoxemic mice, inhibition the activation of EGFR not only decreased TNF-α production in the myocardium but also improved left ventricular pump function and ameliorated cardiac dysfunction and ultimately improved survival rate. All these results provided a new insight of how EGFR regulation the production of TNF-α in cardiomyocytes and a potential new target for the treatment of cardiac dysfunction in sepsis.
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Registered trials
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