ArticleArchives of medical science : AMS2019
The role of interleukin-6 in intracellular signal transduction after chronic β-adrenergic stimulation in mouse myocardium.
Article in Archives of medical science : AMS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
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- Network modeling predicts personalized gene expression and drug responses in valve myofibroblasts cultured with patient sera.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Fibroblast mechanotransduction network predicts targets for mechano-adaptive infarct therapies.eLife · 2022Article
- Role of stilbenes against insulin resistance: A review.Food science & nutrition · 2021Review
- Meta-analysis of transcriptome datasets: An alternative method to study IL-6 regulation in coronavirus disease 2019.Computational and structural biotechnology journal · 2021Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionInflammatory mediators play an important role in development and progression of cardiovascular disease. Both adrenergic stimulation and high levels of interleukin-6 (IL-6) indicate an unfavorable outcome in patients with myocardial infarction or heart failure. Understanding the interaction between β-adrenergic stimulation and IL-6 in the myocardium may contribute to developing more effective treatments. The aim of this study was to verify the role of IL-6 in the effects of β-adrenergic stimulation in activating selected intracellular signaling pathways in mouse myocardium. MATERIAL AND
methodsExperiments were performed on 12-week-old male mice: 16 C57BL/6JIL6
resultsChronic ISO treatment leads to increased fibrosis of the myocardium in mice lacking IL-6, which is accompanied by increased activity of ERK1/2, p38 and reduced expression of SOCS3. Administration of ISO in IL-6 KO animals intensified gene expression of proteins activated by MAPK/ERK (myc; CEBPB; BMP4; Fasn; Tank), while it reduced expression of genes repressed by ERK 1/2 (Wisp1, Wnt1).
conclusionsIL-6 plays an important role in regulating the activation of MAPK pathways in the mouse myocardium in response to chronic β-adrenergic stimulation.
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