Fibrogenesis
Fibrogenesis - Related Videos
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.
08:46
An Improved Method for Rapid Intubation of the Trachea in Mice
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Cited by 24 •
2016
This article presents a rapid and simple method for administering bleomycin directly into the mouse trachea via intubation. Key advantages of this method are that it is highly reproducible, easy to master, and does not require specialized equipment or lengthy recovery times.
07:27
The Murine Choline-Deficient, Ethionine-Supplemented (CDE) Diet Model of Chronic Liver Injury
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Cited by 14 •
2017
Here we describe a common method to induce chronic liver injury in mice by feeding of a choline-deficient and ethionine-supplemented (CDE) diet. We demonstrate health monitoring, liver perfusion, isolation, and preservation. A time course of six weeks can inform about liver injury, pathohistology, fibrosis, inflammatory, and liver progenitor cell responses.
FAQs
Transforming growth factor beta acts as a signaling molecule that activates fibroblasts and promotes their conversion into contractile myofibroblasts. These cells then secrete collagen and other extracellular matrix components. This sequence connects persistent injury or inflammation with structural remodeling, making the signaling pathway important for understanding how a repair response can progress toward excessive scar formation.
When injury or inflammation persists, matrix production may continue instead of resolving after repair. Excessive deposition can then distort the normal organization of tissue, rather than simply closing a damaged area. Such structural disruption can impair organ function, explaining why persistent fibrogenesis contributes to disease in organs including the liver, lungs, kidneys, and heart.
Normal repair includes connective-tissue accumulation and remodeling as part of wound healing. Pathological scarring develops when the response remains unresolved and matrix deposition becomes excessive. The critical difference is therefore not the presence of repair-related tissue remodeling, but whether the process is appropriately controlled or continues long enough to distort tissue structure and reduce organ performance.
Research commonly considers fibrogenesis in the liver, lungs, kidneys, and heart because excessive extracellular matrix deposition can affect each organ’s structure and function. Examining these different tissues helps relate a shared biological process to distinct disease settings. It also supports investigation of how persistent injury or inflammation produces organ-specific consequences through abnormal tissue remodeling.
Investigating the signaling and cellular events in fibrogenesis helps researchers identify measurable indicators associated with abnormal tissue remodeling. Biomarkers can provide evidence of disease mechanisms or fibrotic activity, although the overview does not specify particular markers or testing procedures. This research direction is valuable because it can improve the assessment of disease processes alongside structural and functional changes.
The central therapeutic goal is to limit pathological scarring without eliminating the connective-tissue response required for normal repair. Researchers therefore evaluate approaches that reduce excessive matrix deposition while preserving useful wound-healing activity. This balance matters because suppressing the process indiscriminately could interfere with repair, whereas controlling unresolved activity may help protect organ structure and function.