Hypertrophic Scars
Hypertrophic Scars - Related Videos
05:54
A Mouse Model of Mechanotransduction-driven, Human-like Hypertrophic Scarring
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Cited by 3 •
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.
08:20
In Vitro Model of Human Cutaneous Hypertrophic Scarring using Macromolecular Crowding
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Cited by 8 •
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.
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.
01:29
Cardiomyopathy III: Hypertrophic Cardiomyopathy
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2025
Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
03:45
Investigating the Pathogenesis of MYH7 Mutation Gly823Glu in Familial Hypertrophic Cardiomyopathy using a Mouse Model
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Cited by 4 •
2022
Based on the familial hereditary cardiomyopathy family found in our clinical work, we created a C57BL/6N mouse model with a point mutation (G823E) at the mouse MYH7 locus through CRISPR/Cas9-mediated genome engineering to verify this mutation.
FAQs
Persistent inflammation can keep wound-healing signals active after skin damage, supporting continued fibroblast and myofibroblast activity. This sustained cellular response is associated with transforming growth factor beta signaling, increased collagen deposition, and tissue contraction during remodeling. Examining these linked processes helps biologists understand how repair becomes dysregulated rather than progressing toward controlled tissue restoration.
Fibroblasts and myofibroblasts contribute to the excessive extracellular matrix and contraction that characterize abnormal repair. When their activity remains elevated, collagen deposition and tissue contraction can continue during remodeling, producing firm tissue and potentially limiting movement. Their behavior therefore provides an important cellular focus for studying how wound closure shifts toward fibrosis.
The relationship between the scar and the original injury provides a key distinction. Hypertrophic scars typically remain within the boundaries of the damaged area, whereas the overview identifies comparison with keloids as an important biological question. Researchers can therefore examine scar extent alongside inflammatory activity, matrix deposition, and remodeling behavior when characterizing dysregulated repair.
A useful investigation considers the sequence from persistent inflammation through fibroblast and myofibroblast activity, transforming growth factor beta signaling, collagen deposition, and tissue contraction. Researchers can relate these features to the scar’s location relative to the original injury and to symptoms such as itching, pain, or restricted movement. This integrated view connects molecular activity with tissue-level outcomes.
Burns, surgery, and trauma are particularly relevant settings because the overview identifies them as situations in which these scars may develop. Studying samples or cases from such injuries can help connect the extent of skin damage with later remodeling, excessive matrix production, contraction, and symptoms. These contexts also support evaluation of strategies intended to limit fibrosis while preserving wound closure.
Intervention studies can focus on whether fibrosis is reduced without disrupting effective wound closure. Relevant outcomes include changes in persistent inflammation, fibroblast and myofibroblast activity, transforming growth factor beta signaling, collagen deposition, tissue contraction, and symptoms such as itching, pain, or reduced movement. Comparing these outcomes helps determine whether an approach addresses dysregulated repair rather than only its appearance.