ArticleExperimental and therapeutic medicine2016
Effect of AMP-activated protein kinase activation on cardiac fibroblast proliferation induced by coxsackievirus B3.
Article in Experimental and therapeutic medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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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Who cites it
4 citing papers in PubMed.
- Targeting the Myocardial Microenvironment: Novel Antiviral Strategies and Therapeutic Perspectives for Coxsackievirus B-Induced Myocarditis.Journal of the American Heart Association · 2026Review
- Mechanisms and Therapeutic Strategies of Viral Myocarditis Targeting Autophagy.Frontiers in pharmacology · 2022Review
- Akt inhibitor deguelin aggravates inflammation and fibrosis in myocarditis.Iranian journal of basic medical sciences · 2019Article
- Cardiac Proteome Profiling in Ischemic and Dilated Cardiomyopathy Mouse Models.Frontiers in physiology · 2019Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excessive fibroblast proliferation and collagen production are the major pathogenic mechanisms in the progression of viral myocarditis, which is most frequently associated with infection by coxsackievirus B3 (CVB3). AMP-activated protein kinase (AMPK) has been confirmed to be involved in the progression of myocardial remodeling. However, it remains unclear whether AMPK has an effect on CVB3-induced cardiac fibroblast proliferation. In the present study, the effects of AMPK on cardiac fibroblast proliferation and collagen secretion induced by CVB3 were investigated. Proliferation of neonatal cardiac fibroblasts was determined by cell counting and detection of newly synthesized DNA in cells, and the proportion of cells in the S phase was measured. Hydroxyproline ELISA was used to detect collagen secretion. Phosphorylation of AMPKα-Thr
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