ReviewJournal of molecular and cellular cardiology2016
Computational modeling of cardiac fibroblasts and fibrosis.
Review in Journal of molecular and cellular cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
44 citing papers in PubMed, 63 citations in OpenAlex.
- Computational modeling identifies protective mechanisms of estrogen and testosterone against atrial fibrosis.American journal of physiology. Heart and circulatory physiology · 2026Article
- ECMSim: A high-performance interactive web application for real-time spatiotemporal simulation of cardiac ECM signaling and diffusion.Matrix biology plus · 2026Article
- Cardiac fibroblasts in myocardial injury and heart failure.European heart journal · 2026Review
- T-World Virtual Human Cardiomyocyte. II. Organ-Scale Simulations and Applications.Circulation research · 2026Article
- AI-based Predictive Signaling Pathway Profiling in Cardiac Fibrosis Suggests a Novel Combinatorial Treatment Strategy.bioRxiv : the preprint server for biology · 2025Article
- Computational modelling of cardiac fibroblast signalling reveals a key role for CaThe Journal of physiology · 2025Article
- A rule-based multiscale model of hepatic stellate cell plasticity: Critical role of the inactivation loop in fibrosis progression.PLoS computational biology · 2024Article
- Review
- Diversity of cells and signals in the cardiovascular system.The Journal of physiology · 2023Article
- Combining Cell Technologies With Biomimetic Tissue Engineering Applications: A New Paradigm for Translational Cardiovascular Therapies.Stem cells translational medicine · 2023Review
- The physics of heart rhythm disorders.Physics reports · 2022Article
- On modeling the multiscale mechanobiology of soft tissues: Challenges and progress.Biophysics reviews · 2022Review
- 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
- Neutrophil crosstalk during cardiac wound healing after myocardial infarction.Current opinion in physiology · 2021Article
- Review
- Effects of Sex and 17 β-Estradiol on Cardiac Fibroblast Morphology and Signaling Activities In Vitro.Cells · 2021Article
- Multiscale modeling in disease.Current opinion in systems biology · 2021Article
- Mechano-chemo signaling interactions modulate matrix production by cardiac fibroblasts.Matrix biology plus · 2021Article
- Model Systems for Addressing Mechanism of Arrhythmogenesis in Cardiac Repair.Current cardiology reports · 2021Review
- Network model-based screen for FDA-approved drugs affecting cardiac fibrosis.CPT: pharmacometrics & systems pharmacology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Altered fibroblast behavior can lead to pathologic changes in the heart such as arrhythmia, diastolic dysfunction, and systolic dysfunction. Computational models are increasingly used as a tool to identify potential mechanisms driving a phenotype or potential therapeutic targets against an unwanted phenotype. Here we review how computational models incorporating cardiac fibroblasts have clarified the role for these cells in electrical conduction and tissue remodeling in the heart. Models of fibroblast signaling networks have primarily focused on fibroblast cell lines or fibroblasts from other tissues rather than cardiac fibroblasts, specifically, but they are useful for understanding how fundamental signaling pathways control fibroblast phenotype. In the future, modeling cardiac fibroblast signaling, incorporating -omics and drug-interaction data into signaling network models, and utilizing multi-scale models will improve the ability of in silico studies to predict potential therapeutic targets against adverse cardiac fibroblast activity.
Indexed as
Identifiers
What Socratic holds
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.