Mouse Fibrosis Model
Mouse Fibrosis Model - Related Videos
06:26
Mouse Model of Metabolic Dysfunction-Associated Steatotic Liver Disease with Fibrosis
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Cited by 1 •
2025
Mouse model of metabolic dysfunction-associated steatotic liver disease (MASLD) with metabolic dysfunction, hepatic gene expression changes, and liver histopathological alterations that resemble human MASLD, including fibrosis that progresses to advanced fibrosis stage 3. This model can be used in studies of MASLD pathophysiology and in pre-clinical studies of new therapies.
09:44
Evaluating Therapeutic Interventions in the SHIP-deficient Mouse Model of Crohn Disease-like Ileitis and Fibrosis
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2025
This protocol demonstrates how the Src homology 2 domain-containing 5'-inositol phosphatase (SHIP)-deficient mouse model of Crohn disease (CD)-like ileal inflammation and fibrosis can be used to test novel therapeutics for CD.
05:45
A Refined Aerosol-Based Intratracheal Bleomycin Delivery Method for Reproducible and Minimally Invasive Mouse Models of Pulmonary Fibrosis
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2026
Here, we present a protocol to model pulmonary fibrosis in mice using aerosolized bleomycin delivered via the trachea. This optimized method enables uniform, quantitative, and precise delivery without surgical incision, enhancing the reproducibility and reliability of bleomycin-induced fibrosis.
09:27
The Dimethylnitrosamine Induced Liver Fibrosis Model in the Rat
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Cited by 11 •
2016
We describe a method to produce an animal model of liver fibrosis in the rat, and assess the degree of fibrosis by histological examination of the liver. The model can be used to study the development of liver disease as well as to test the efficacy of potential anti-fibrotic agents.
09:12
A Mouse Model of Chronic Liver Fibrosis for the Study of Biliary Atresia
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Cited by 3 •
2023
We established a mouse model of chronic liver fibrosis, which provides a suitable animal model for the virus-induced liver fibrosis mechanistic study of biliary atresia (BA) and a platform for future BA treatments.
FAQs
Activated fibroblasts, immune cells, and signaling pathways form an interacting system rather than isolated drivers. Persistent injury can maintain inflammatory activity, while pathway changes support fibroblast activation and extracellular matrix accumulation. Examining these relationships helps researchers connect cellular events with collagen deposition and tissue remodeling, clarifying how fibrosis progresses within the selected organ.
Chemical, surgical, infectious, and genetic induction approaches provide alternative ways to establish fibrosis in a defined organ. Their value is not that they are interchangeable, but that they let investigators examine pathological scar formation under different experimental conditions. Selecting among them can align the model with the mechanism, tissue, or intervention being studied.
Repeated assessment captures how fibrosis develops instead of treating it as a static lesion. Researchers can follow changes in collagen accumulation, tissue remodeling, and organ structure or function over time, while relating those outcomes to ongoing injury, inflammation, fibroblast activation, and signaling activity. This temporal view can reveal when an intervention changes disease-associated processes.
A useful evaluation combines biological, structural, and functional readouts. Investigators can examine activated fibroblasts, immune cells, signaling pathways, collagen accumulation, and tissue remodeling, then compare these findings with changes in organ structure and function. Using several readout categories links cellular mechanisms with the broader tissue consequences of fibrosis in the affected organ.
In medicine, these models support the evaluation of antifibrotic therapies, biomarkers, and targeted interventions. The framework can be applied to liver, lung, kidney, and cardiac fibrosis, allowing investigators to ask whether a treatment or marker tracks with collagen accumulation, tissue remodeling, or broader structural and functional changes in the affected organ.
Findings from a mouse system should not be transferred to patients without qualification. Biological differences between mice and humans make translation a central interpretive issue. Results are most informative when researchers distinguish evidence obtained in the selected organ and model from conclusions about human disease, treatment response, or biomarker performance.