ArticleScientific reports2022
Computational simulation of liver fibrosis dynamics.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Towards Bayesian-based quantitative adverse outcome pathways using in vitro data from open literature and continuous variables: a case example for liver fibrosis.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Lumped parameter modeling of changes in liver hemodynamics due to cirrhosis.Biomechanics and modeling in mechanobiology · 2026Article
- Reduction in Hepatic Phosphatidylcholine Biosynthesis Promotes MASH Through Copper Deficiency.bioRxiv : the preprint server for biology · 2026Article
- Towards linking histological changes to liver viscoelasticity: a hybrid analytical-computational micromechanics approach.Physics in medicine and biology · 2025Article
- Article
- A rule-based multiscale model of hepatic stellate cell plasticity: Critical role of the inactivation loop in fibrosis progression.PLoS computational biology · 2024Article
- Hepatic microcirculatory disturbance in liver diseases: intervention with traditional Chinese medicine.Frontiers in pharmacology · 2024Review
- The 3Rs in Experimental Liver Disease.Animals : an open access journal from MDPI · 2023Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Liver fibrosis is a result of homeostasis breakdown caused by repetitive injury. The accumulation of collagens disrupts liver structure and function, which causes serious consequences such as cirrhosis. Various mathematical simulation models have been developed to understand these complex processes. We employed the agent-based modelling (ABM) approach and implemented inflammatory processes in central venous regions. Collagens were individually modelled and visualised depending on their origin: myofibroblast and portal fibroblast. Our simulation showed that the administration of toxic compounds induced accumulation of myofibroblast-derived collagens in central venous regions and portal fibroblast-derived collagens in portal areas. Subsequently, these collagens were bridged between central-central areas and spread all over areas. We confirmed the consistent dynamic behaviour of collagen formulation in our simulation and from histological sections obtained via in vivo experiments. Sensitivity analyses identified dead hepatocytes caused by inflammation and the ratio of residential liver cells functioned as a cornerstone for the initiation and progression of liver fibrosis. The validated mathematical model demonstrated here shows virtual experiments that are complementary to biological experiments, which contribute to understanding a new mechanism of liver fibrosis.
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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.