Cachexia-induced Wat Remodeling
Cachexia-induced Wat Remodeling - Related Videos
08:55
The Colon-26 Carcinoma Tumor-bearing Mouse as a Model for the Study of Cancer Cachexia
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Cited by 111 •
2016
Mice bearing the Colon-26 (C26) carcinoma represent a classical model of cancer cachexia. Progressive muscle wasting occurs in association with tumor growth, over-expression of muscle-specific ubiquitin ligases, and reductions in muscle cross-sectional area. Fat loss is also observed. Cachexia is studied in a time-dependent manner with increasing severity of wasting.
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.
02:58
Nanoparticle-Mediated Visualization of Endo-Lysosomal Remodeling in Bacterially-Infected Cells
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2025
Source: Zhang, Y., et al. Application of Fluorescent Nanoparticles to Study Remodeling of the Endo-lysosomal System by Intracellular Bacteria. J. Vis. Exp. (2015)This video demonstrates the use of fluorescent nanoparticles to visualize endo-lysosomal remodeling in human epithelial cells infected by intracellular bacteria. Following bacterial invasion, the pathogens manipulate the host cytoskeleton and endo-lysosomal system, forming vacuoles with tubular projections that alter vesicle transport.
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
Signals originating from tumors or inflammatory processes can activate lipolysis in adipocytes, causing stored lipids to be mobilized rather than retained. This shift changes the contribution of WAT to whole-body energy balance and can accelerate adipose depletion. In cachexia biology, it links disease-associated signaling to progressive loss of fat reserves.
Extracellular matrix changes indicate that the adipose tissue environment is being reorganized alongside adipocyte metabolism. In cachexia, tumor- or inflammation-associated signals can promote these changes, so the tissue response includes both altered cellular energy handling and structural modification of the fat depot. This broader view shows that remodeling is a tissue-level process, not only a reduction in fat mass.
Beige-cell conversion changes WAT from primarily energy storage toward thermogenic activity. Because thermogenesis uses energy, this shift can raise energy expenditure within the remodeling depot and contribute to ongoing lipid and fat loss. Its importance in cachexia is that adipose tissue can participate actively in the energy imbalance associated with progressive wasting.
Cachexia-induced WAT remodeling can combine mobilization of stored lipids with greater energy use by thermogenic cells. Lipolysis reduces the tissue’s energy-storage function, while beige-cell activity increases expenditure. Considering both processes together helps explain how adipose changes may contribute to systemic metabolic imbalance rather than acting as an isolated local defect.
Examining WAT remodeling gives researchers a tissue-specific way to connect disease signals with whole-body consequences. Relevant features include adipocyte lipolysis, extracellular matrix alteration, beige-cell conversion, fat-depot loss, and increased energy expenditure. Taken together, these changes can clarify how cachexia progresses and why metabolic imbalance accompanies depletion of adipose reserves.
Research on this process may support biomarkers that reflect cachexia-associated adipose changes and therapies aimed at preserving WAT. Such approaches are relevant because limiting tissue deterioration could address more than visible fat loss: they may help reduce metabolic disruption and improve treatment tolerance. These possibilities are goals of studying remodeling, not established clinical outcomes.