ArticleBiology open2020
Short-term cyclical stretch phosphorylates p38 and ERK1/2 MAPKs in cultured fibroblasts from the hearts of rainbow trout,
Article in Biology open, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 10 citations in OpenAlex.
- De Novo Genome Assemblies of Four Rainbow Trout Genetic Lines Reveal Structural Variants in Pursuit of a Pangenome Reference.Molecular ecology resources · 2026Article
- Integrated response of the zebrafish (Danio rerio) cardiovascular system to hypoxia acclimation.The Journal of experimental biology · 2025Article
- Comparative analysis of ventricular stiffness across species.Physiological reports · 2024Review
- Regulation of collagen deposition in the trout heart during thermal acclimation.Current research in physiology · 2022Article
- Mitogen-activated protein kinases contribute to temperature-induced cardiac remodelling in rainbow trout (Oncorhynchus mykiss).Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2022Article
- Channelling the Force to Reprogram the Matrix: Mechanosensitive Ion Channels in Cardiac Fibroblasts.Cells · 2021Review
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
The form and function of the rainbow trout heart can remodel in response to various stressors including changes in environmental temperature and anemia. Previous studies have hypothesized that changes in biomechanical forces experienced by the trout myocardium as result of such physiological stressors could play a role in triggering the remodeling response. However, there has been no work examining the influence of biomechanical forces on the trout myocardium or of the cellular signals that would translate such a stimuli into a biological response. In this study, we test the hypothesis that the application of biomechanical forces to trout cardiac fibroblasts activate the cell signaling pathways associated with cardiac remodeling. This was done by cyclically stretching cardiac fibroblasts to 10% equibiaxial deformation at 0.33 Hz and quantifying the activation of the p38-JNK-ERK mitogen activated protein kinase (MAPK) pathway. After 20 min, p38 MAPK phosphorylation was elevated by 4.2-fold compared to control cells (
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Registered trials
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