ArticleMolecular medicine reports2017
Coxsackieviruses B3 infection of myocardial microvascular endothelial cells activates fractalkine via the ERK1/2 signaling pathway.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 5 citations in OpenAlex.
- Targeting the Myocardial Microenvironment: Novel Antiviral Strategies and Therapeutic Perspectives for Coxsackievirus B-Induced Myocarditis.Journal of the American Heart Association · 2026Review
- Virus-induced endothelial senescence as a cause and driving factor for ME/CFS and long COVID: mediated by a dysfunctional immune system.Cell death & disease · 2026Review
- Identification of Drug Repurposing Candidates for Coxsackievirus B3 Infection in iPSC-Derived Brain-like Endothelial Cells.International journal of molecular sciences · 2025Article
- Sex Differences in Expression of Pro-Inflammatory Markers and miRNAs in a Mouse Model of CVB3 Myocarditis.International journal of molecular sciences · 2024Article
- An Approach to Biomarker Discovery of Cannabis Use Utilizing Proteomic, Metabolomic, and Lipidomic Analyses.Cannabis and cannabinoid research · 2022Article
- The MEK inhibitor U0126 ameliorates diabetic cardiomyopathy by restricting XBP1's phosphorylation dependent SUMOylation.International journal of biological sciences · 2021Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infections by pathogens may lead to cardiovascular diseases, including acute/chronic myocarditis. (Coxsackieviruses B3) CVB3 is considered to be the most common causative agent in m‑yocarditis, which can lead to dilated cardiomyopathy. The present study aimed to investigate the mechanism of CVB3‑infected myocardial microvascular endothelial cells. The CVB3 infection was detected by 50% tissue culture infective dose (TCID50). The role of fractalkine (FKN) in the infection was detected using western blotting and RNA interference. To assess mitogen‑activated protein kinase signaling activity, levels of total and phosphorylated extracellular signal‑regulated kinase (ERK)1/2, c‑Jun N‑terminal kinase, and p38 were measured at 0, 20, 40, and 60 min after CVB3 infection by western blot analysis. The results showed that infection activated FKN via the ERK1/2 signaling pathway. Furthermore, the TCID50 of CVB3 in infected cells was lower compared with that in myocardial microvascular endothelial cells following ERK1/2 inhibition and FKN silencing. CVB3 infection of myocardial microvascular endothelial cells activates FKN via the ERK1/2 signaling pathway. These findings represent a foundation for the development of novel methods of treating CVB3‑induced myocarditis.
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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 Socratic graph.