Fibrotic Changes
Fibrotic Changes - Related Videos
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 7 •
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.
09:16
Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
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Cited by 7 •
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.
02:49
Picrosirius Red Polarization Staining: A Technique To Detect Fibrosis in Cardiac Tissue Sections Using Bright-Field Microscopy
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2025
This video describes the picrosirius red staining of fibrotic tissues to detect excessive collagen deposition in fibrotic tissue sections. The staining technique helps assess collagen expression in connective-tissue diseases.
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.
06:47
Isolation of Mesenchymal Stem Cells from Human Alveolar Periosteum and Effects of Vitamin D on Osteogenic Activity of Periosteum-derived Cells
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Cited by 15 •
2018
We present a protocol to investigate the mRNA expression biomarkers of periosteum-derived cells (PDCs) induced by vitamin C (vitamin C) and 1,25-dihydroxy vitamin D [1,25-(OH)2D3]. In addition, we evaluate the ability of PDCs to differentiate into osteocytes, chondrocytes, and adipocytes.
FAQs
Persistent injury or inflammation keeps repair signals active instead of allowing the tissue to return to normal. These signals activate fibroblasts and myofibroblasts, which increase production and deposition of extracellular matrix proteins, especially collagen. When matrix accumulation outpaces removal, the tissue progressively remodels and loses its original organization, creating a biological basis for chronic scarring.
Limited matrix deposition can support wound repair by stabilizing damaged tissue while healing occurs. Fibrotic changes become harmful when matrix production continues or removal cannot keep pace, causing scar material to accumulate. The resulting stiffening can interfere with normal tissue structure and function, so the balance between repair and resolution is central to determining whether scarring remains adaptive or becomes pathological.
Fibroblasts and myofibroblasts are key cellular sources of the excess extracellular matrix associated with scarring. Their activation links persistent inflammation to collagen accumulation and tissue remodeling. Studying these cells helps biologists explain how fibrosis progresses and supports treatment strategies aimed at reducing matrix production rather than addressing inflammation alone.
The consequences depend on where excessive matrix accumulates and how much it alters the local structure. In the liver, lungs, heart, and kidneys, progressive scarring can stiffen tissue and disrupt normal organ function. This organ-wide perspective matters because the same general remodeling process may produce different biological and functional consequences at different sites.
Research on fibrotic changes can reveal how chronic injury, inflammation, cellular activation, and extracellular matrix remodeling interact over time. It can also help identify biomarkers associated with tissue remodeling, providing measurable indicators of disease-related structural change. These findings connect cellular mechanisms with organ dysfunction and guide investigation of approaches that may limit or reverse pathological scarring.
Three major intervention directions are highlighted by fibrosis biology: reducing persistent inflammation, limiting excessive extracellular matrix production, and promoting scar resolution. These strategies address different stages of the process, from the signals that activate fibroblasts and myofibroblasts to the imbalance between matrix deposition and removal. Comparing them helps researchers determine how best to restore healthier tissue remodeling.