Fibrosis Remodeling
Fibrosis Remodeling - Related Videos
02:54
Nucleosome Remodeling
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2020
Nucleosomes are the basic units of chromatin compaction. Each nucleosome consists of the DNA bound tightly around a histone core, which makes the DNA inaccessible to DNA binding proteins such as DNA polymerase and RNA polymerase. Hence, the fundamental problem is to ensure access to DNA when appropriate, despite the compact and protective chromatin structure. Nucleosome remodeling complex Eukaryotic cells have specialized enzymes called ATP-dependent nucleosome remodeling enzymes. These enzymes...
07:31
A Model of Cardiac Remodeling Through Constriction of the Abdominal Aorta in Rats
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Cited by 26 •
2016
A rat model of abdominal aortic constriction that induces cardiac hypertrophy and remodeling is described. An efficient, highly-reproducible, and minimally-invasive method is used to provide a simple yet useful platform for research in myocardial hypertrophy and dysfunction.
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.
01:40
Bone Remodeling
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2025
Bone remodeling is a continuous and balanced process of bone resorption by osteoclasts and bone formation by osteoblasts. In adults, it helps maintain bone mass and calcium homeostasis. While mechanical stress can stimulate turnover as part of the normal maintenance and reparative process, several hormones also regulate bone remodeling. Hormonal Control of Bone Remodeling Parathyroid hormone (PTH) maintains homeostatic control of blood calcium levels by regulating bone resorption. PTH is...
10:14
Biochemical Assays for Analyzing Activities of ATP-dependent Chromatin Remodeling Enzymes
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Cited by 4 •
2014
Here we describe biochemical assays that can be used to characterize ATP-dependent chromatin remodeling enzymes for their abilities to 1) catalyze ATP-dependent nucleosome sliding, 2) engage with nucleosome substrates, and 3) hydrolyze ATP in a nucleosome- or DNA-dependent manner.
FAQs
The transition from fibroblast to myofibroblast is a key control point because myofibroblasts produce extracellular matrix. Their activation can increase scar-tissue accumulation and influence whether repair remains temporary or progresses toward persistent fibrosis. In biological studies, tracking this cellular change helps connect cell behavior with later alterations in collagen architecture, tissue mechanics, and tissue function.
Collagen deposition adds structural material to the extracellular matrix, while cross-linking can make that matrix more organized and persistent. These changes affect the physical properties of scar tissue and may alter tissue mechanics. Examining both processes helps researchers determine how an initially reparative matrix becomes associated with excessive scarring and impaired tissue function.
Proteolytic enzymes and other participating cells contribute to matrix degradation and reorganization after matrix deposition. Their activity can modify the amount, arrangement, and persistence of scar tissue rather than simply removing it. Studying this remodeling phase is important because the balance between matrix production and breakdown helps determine whether fibrosis resolves, remains stable, or continues progressing.
Temporary repair is associated with a wound-healing response that can be remodeled, whereas persistent fibrosis reflects continued or excessive scarring during chronic disease. The distinction depends on the duration and balance of matrix production, collagen organization, degradation, and reorganization. This comparison helps biology researchers relate cellular and extracellular-matrix changes to disease progression in affected organs.
A useful investigation follows several connected features: fibroblast activation, myofibroblast-associated matrix production, collagen deposition and cross-linking, and subsequent matrix degradation or reorganization. Researchers can then relate these changes to tissue mechanics, disease progression, biomarkers, or tissue function. Organizing observations across these stages clarifies how cellular activity produces broader structural and biological outcomes.
The process can be examined in organs identified as vulnerable to pathological scarring, including the liver, lung, heart, and kidney. Comparing these settings helps researchers ask whether similar matrix and cellular changes accompany disease progression in different tissues. Such comparisons also support investigation of organ-specific consequences, biomarkers, and strategies intended to limit scarring or restore function.
Studying fibrosis remodeling supports several applications in biology: analyzing tissue mechanics, following disease progression, identifying biomarkers, and evaluating therapies designed to limit pathological scarring or restore tissue function. The remodeling framework is especially useful because it connects cellular activation and matrix restructuring with measurable disease-related outcomes, providing context for both mechanistic research and therapeutic investigation.