Fibrotic Scar
Fibrotic Scar - Related Videos
07:40
Visualizing Scar Development Using SCAD Assay - An Ex-situ Skin Scarring Assay
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2022
This protocol describes the generation of a skin-fascia explant termed "SCar like tissue in A Dish" or SCAD. This model allows unprecedented visualization of single fibroblasts during scar formation.
05:54
A Mouse Model of Mechanotransduction-driven, Human-like Hypertrophic Scarring
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Cited by 4 •
2024
This protocol will explain how to establish a hypertrophic scarring murine model that increases mechanotransduction signaling to simulate human-like scarring. This method involves increasing mechanical tension across a healing incision in a mouse and using a specialized device to create reproducible, excessive scar tissue for detailed histological and bioinformatic analyses.
10:42
Development of an Ethanol-induced Fibrotic Liver Model in Zebrafish to Study Progenitor Cell-mediated Hepatocyte Regeneration
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Cited by 8 •
2016
Sustained fibrosis with deposition of excessive extracellular matrix proteins leads to cirrhosis. Alcohol abuse is one of the main causes of severe liver disease. We established an ethanol-induced zebrafish fibrotic liver model to study the mechanisms and strategies of promoting hepatocyte regeneration upon alcohol-induced injury.
08:20
In Vitro Model of Human Cutaneous Hypertrophic Scarring using Macromolecular Crowding
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Cited by 9 •
2020
This protocol describes the use of macromolecular crowding to create an in vitro human hypertrophic scar tissue model that resembles in vivo conditions. When cultivated in a crowded macromolecular environment, human skin fibroblasts exhibit phenotypes, biochemistry, physiology, and functional characteristics resembling scar tissue.
09:16
Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
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Cited by 6 •
2018
Here we present a robust method to reprogram primary embryonic fibroblasts into functional cardiomyocytes through overexpression of GATA4, Hand2, Mef2c, Tbx5, miR-1, and miR-133 (GHMT2m) alongside inhibition of TGF-β signaling. Our protocol generates beating cardiomyocytes as early as 7 days post-transduction with up to 60% efficiency.
FAQs
Persistent inflammatory signals activate fibroblasts and myofibroblasts after injury, shifting healing toward continued extracellular matrix production. These cells deposit collagen and other matrix components, increasing tissue density and altering its mechanical properties. In bioengineering studies, modeling this cellular response helps researchers examine how prolonged repair signaling contributes to impaired tissue structure and function.
Transforming growth factor beta acts as an important signal influencing fibroblast and myofibroblast behavior during wound healing. Its activity is associated with increased deposition of collagen and other extracellular matrix components. Studying this pathway helps bioengineers evaluate how signaling conditions promote excessive matrix accumulation and identify experimental strategies for assessing antifibrotic interventions.
Scar persistence depends not only on new matrix production but also on whether existing matrix is removed. When degradation is inadequate, collagen and other extracellular matrix components remain accumulated rather than being sufficiently cleared. This imbalance can stabilize the altered tissue region, making matrix persistence a central variable in engineered models of fibrotic remodeling.
A fibrotic scar has altered mechanical properties because excessive extracellular matrix changes the surrounding tissue environment. Bioengineered systems can reproduce these stiffness changes alongside associated cell behavior, allowing researchers to study the relationship between physical matrix conditions and cellular responses. This connection is useful when designing models that more closely represent fibrotic tissue than simple cell cultures.
Researchers use biomaterials and tissue-engineered constructs to recreate selected features of fibrotic tissue, including excessive matrix deposition and altered mechanical conditions. These platforms provide controlled settings for examining how cells respond to the engineered environment. They can therefore support systematic evaluation of fibrotic processes and potential interventions without relying only on naturally formed scar tissue.
Organ-on-chip models provide another bioengineering platform for reproducing changes in matrix stiffness and cell behavior associated with fibrotic scars. By combining these features in an engineered system, researchers can investigate tissue responses under defined conditions. Such models help connect cellular mechanisms with tissue-level dysfunction and support testing of approaches intended to reduce or manage fibrosis.
Biomaterials, tissue-engineered constructs, and organ-on-chip systems can be designed to reproduce key fibrotic features, including altered matrix mechanics and cell behavior. Researchers can then use these models to evaluate antifibrotic therapies in a controlled experimental context. The resulting observations may clarify whether an intervention affects the processes that maintain excessive extracellular matrix accumulation.
Fibrotic scar research helps bioengineers account for excessive matrix formation and mechanical alteration when designing implants or tissue-engineered systems. Understanding these responses can guide strategies intended to limit impaired tissue structure and function around engineered tissues. The broader goal is to improve implant design and support regeneration that restores tissue performance rather than stabilizing a dysfunctional scar.