Stromal Fibrosis
Stromal Fibrosis - Related Videos
08:37
Isolation of Mouse Endometrial Epithelial and Stromal Cells for In Vitro Decidualization
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Cited by 86 •
2017
This study presents a standardized and validated method for the isolation and culture of primary mouse endometrial stromal and epithelial cells, which can be used in a coculture system to study in vitro decidualization.
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.
01:23
Cystic Fibrosis: Pathogenesis
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2024
Cystic fibrosis (CF), an autosomal recessive disorder, significantly affects the function of exocrine glands. This genetically inherited disease is characterized by the production of thick and sticky mucus, which can severely affect various organs and systems in the body. CF is primarily caused by a genetic mutation in a chromosome 7 gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. The most common gene mutation leading to CF is the ΔF508 mutation, but...
05:52
An In Vitro Flow Investigation of the Effect of Stromal Cells on Leukocyte Recruitment
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2025
The video demonstrates a method for investigating the impact of stromal cells on leukocyte recruitment. In a parallel plate flow chamber model, pro-inflammatory cytokines induce the expression of adhesion receptors by endothelial cells, facilitating neutrophil recruitment and migration. The cross-talk between stromal cells and endothelial cells diminishes neutrophil recruitment to the endothelial cells.
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.
FAQs
Chronic injury or inflammation can keep fibroblasts and myofibroblasts activated. These cells produce and remodel extracellular matrix proteins, including collagen. Progression occurs when matrix production and deposition outpace matrix breakdown, allowing scar tissue to accumulate and progressively disrupt tissue architecture and normal function over time.
Matrix remodeling determines whether connective tissue accumulation stabilizes or expands. When extracellular matrix deposition exceeds breakdown, the balance shifts toward persistent scar formation. This imbalance can change the physical environment of affected tissue, helping explain why fibrosis may progressively interfere with architecture rather than remain a temporary response to injury.
Increased tissue stiffness can alter cell behavior, blood flow, and treatment response. In tumors, these effects make the stromal environment biologically important rather than merely structural. Assessing stiffness-related changes therefore helps connect matrix accumulation with disease behavior and therapeutic performance, especially when fibrosis accompanies malignant tissue remodeling.
Stromal fibrosis is medically relevant in the liver, lung, heart, and kidney, and it also occurs in tumors. In each setting, accumulated matrix can impair tissue architecture and function, while altered stiffness may influence blood flow, cell behavior, or treatment response. This cross-organ relevance supports fibrosis assessment in disease management and biomedical research.
Histopathology and imaging provide complementary ways to assess the extent and consequences of fibrosis. Histopathology examines affected tissue directly, while imaging evaluates changes in the organ in a clinical or research setting. Together, they can support assessment of fibrotic involvement and its relationship to altered architecture and function without relying on one type of evidence alone.
Current research focuses on limiting matrix production or improving matrix remodeling. These strategies target the imbalance that allows scar tissue to persist, rather than addressing only the original injury. Their broader goal is to reduce the structural consequences of fibrosis and potentially improve how affected tissue behaves or responds to treatment.