ArticleFrontiers in network physiology2024
Elucidating the interaction between stretch and stiffness using an agent-based spring network model of progressive pulmonary fibrosis.
Article in Frontiers in network physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed.
- Mechanical stretch reduces fibroblast activation in heart failure with reduced ejection fraction.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2026Article
- Association ofInternational journal of molecular sciences · 2026Article
- An agent-based model suggests how senescent cell behavior and matrix mechanics drive pulmonary fibrosis in aged mice.bioRxiv : the preprint server for biology · 2026Article
- Modeling ventilation heterogeneity in lung fibrosis.Medical & biological engineering & computing · 2026Article
- Mechanobiology and Resolution of Lung Fibrosis.Annual review of physiology · 2026Review
- Nanocarrier-Enabled siRNA Therapy for Pulmonary Fibrosis: Pharmacological Rationale, Delivery Barriers, and Translational Opportunities.International journal of nanomedicine · 2026Review
- Network-Associated Mechanotransduction in Health and Disease.Results and problems in cell differentiation · 2026Review
- The Extracellular Matrix and the Immune System in Acute Lung Injury: Partners in Damage and Repair.Biomedicines · 2025Review
- Insight into the pathogenesis of interstitial lung diseases and near-to-native lung fibrosis models.European journal of medical research · 2025Review
- Novel murine partial tracheal occlusion model with altered respiratory dynamics.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Multiscale computational model predicts how environmental changes and treatments affect microvascular remodeling in fibrotic disease.PNAS nexus · 2025Article
- Bifurcation in the healing or fibrotic response in a network model of fibrosis: role of the initial injury structure.Frontiers in network physiology · 2025Article
- Digital twins for chronic lung diseases.European respiratory review : an official journal of the European Respiratory Society · 2024Review
- The Fibrotic Phenotype of Human Precision-Cut Lung Slices Is Maintained after Cryopreservation.Toxics · 2024Article
- Physiological network approach to prognosis in cirrhosis: A shifting paradigm.Physiological reports · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Pulmonary fibrosis is a deadly disease that involves the dysregulation of fibroblasts and myofibroblasts, which are mechanosensitive. Previous computational models have succeeded in modeling stiffness-mediated fibroblasts behaviors; however, these models have neglected to consider stretch-mediated behaviors, especially stretch-sensitive channels and the stretch-mediated release of latent TGF-β. Here, we develop and explore an agent-based model and spring network model hybrid that is capable of recapitulating both stiffness and stretch. Using the model, we evaluate the role of mechanical signaling in homeostasis and disease progression during self-healing and fibrosis, respectively. We develop the model such that there is a fibrotic threshold near which the network tends towards instability and fibrosis or below which the network tends to heal. The healing response is due to the stretch signal, whereas the fibrotic response occurs when the stiffness signal overpowers the stretch signal, creating a positive feedback loop. We also find that by changing the proportional weights of the stretch and stiffness signals, we observe heterogeneity in pathological network structure similar to that seen in human IPF tissue. The system also shows emergent behavior and bifurcations: whether the network will heal or turn fibrotic depends on the initial network organization of the damage, clearly demonstrating structure's pivotal role in healing or fibrosis of the overall network. In summary, these results strongly suggest that the mechanical signaling present in the lungs combined with network effects contribute to both homeostasis and disease progression.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.