ArticleCellular and molecular bioengineering2014
Network Modeling Approach to Predict Myofibroblast Differentiation.
Article in Cellular and molecular bioengineering, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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.
The trial behind it
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Who cites it
10 citing papers in PubMed.
- Molecular insights into heart field-specific cardiomyocyte differentiation - A computational study.PloS one · 2026Article
- The mechanopathology of the tumor microenvironment: detection techniques, molecular mechanisms and therapeutic opportunities.Frontiers in cell and developmental biology · 2025Review
- 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
- Mechano-chemo signaling interactions modulate matrix production by cardiac fibroblasts.Matrix biology plus · 2021Article
- Synergistic Effect of Matrix Stiffness and Inflammatory Factors on Osteogenic Differentiation of MSC.Biophysical journal · 2019Article
- Engineering hiPSC cardiomyocyte in vitro model systems for functional and structural assessment.Progress in biophysics and molecular biology · 2019Review
- Mechanical regulation of gene expression in cardiac myocytes and fibroblasts.Nature reviews. Cardiology · 2019Review
- Cellular mechanosensing of the biophysical microenvironment: A review of mathematical models of biophysical regulation of cell responses.Physics of life reviews · 2017Review
- Computational modeling of cardiac fibroblasts and fibrosis.Journal of molecular and cellular cardiology · 2016Review
- Mechanobiology of myofibroblast adhesion in fibrotic cardiac disease.Journal of cell science · 2015Review
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Fibrotic disease is a major cause of morbidity and mortality and is characterized by the transition of resident fibroblast cells into active myofibroblasts, identified by their expression of alpha smooth muscle actin. Myofibroblast differentiation is regulated by growth factor signaling and mechanical signals transduced through integrins, which converge at focal adhesion proteins (Src and FAK) and MAPK signaling, but lead to divergent outcomes. While details are known about individual pathways, little is known about their interactions. To this end, an ODE-based model of this cell signaling network was developed in parallel with
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Registered trials
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