Fibrosis Progression
Fibrosis Progression - Related Videos
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.
08:56
Bile Duct Ligation in Mice: Induction of Inflammatory Liver Injury and Fibrosis by Obstructive Cholestasis
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Cited by 300 •
2015
Disruption of bile flow results in severe inflammatory cholestatic liver injury with a characteristic time-dependent sequence of morphological alterations. Here we present a protocol for the surgical ligation of the common bile duct in mice that allows to induce a strong fibrotic response after 21 to 28 days.
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.
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...
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
Transforming growth factor beta acts as a persistent signaling driver during fibrosis progression. It activates fibroblasts, causing them to become myofibroblasts, which produce collagen and other extracellular matrix components. Continued signaling can therefore sustain matrix accumulation and remodeling rather than allowing tissue structure to return toward its healthier state.
Myofibroblasts are important because they produce the collagen and other extracellular matrix components that accumulate during scarring. Their activity changes the composition and organization of tissue, contributing to progressive remodeling. As this material replaces healthier tissue, the affected organ may lose normal structure and experience reduced function.
Increasing tissue stiffness can reinforce the fibrotic process, creating a feedback relationship between matrix accumulation and continued scarring. As excess connective tissue remodels the affected area, the tissue becomes mechanically altered. That altered environment can further support the process, making progression more persistent and increasing the risk of structural damage.
Chronic injury and inflammation provide conditions that can sustain fibrotic remodeling. When these disturbances persist, signaling pathways such as transforming growth factor beta remain active, supporting fibroblast activation and extracellular matrix production. This helps explain why fibrosis progression is associated with ongoing disease processes rather than only with a single, temporary injury.
Researchers examine fibrosis progression in organs including the liver, lungs, heart, and kidneys to determine how persistent signaling, matrix accumulation, and tissue remodeling relate to organ dysfunction. Comparing these settings helps biology research investigate shared mechanisms while recognizing that the consequences of scarring can differ according to the organ affected.
Fibrosis research uses biomarker identification to help track disease development and evaluate the biological state of affected tissue. Biomarkers can support studies of how scarring changes over time and whether an intervention influences the process. In this context, they are part of efforts to detect progression and assess responses to antifibrotic therapies.
Timing matters because fibrosis progression can produce structural damage that eventually becomes irreversible. Evaluating antifibrotic therapies or other limiting strategies before that stage may help determine whether progression can be reduced while tissue remodeling remains modifiable. This makes early investigation of signaling, biomarkers, and matrix changes important in biology and therapeutic research.