Mouse Cardiac Remodeling
Mouse Cardiac Remodeling - Related Videos
08:25
Visualization of Streptococcus pneumoniae within Cardiac Microlesions and Subsequent Cardiac Remodeling
0 Views •
Cited by 11 •
2015
Streptococcus pneumoniae forms discrete non-purulent microscopic lesions in the heart. Outlined is the protocol for a murine model of cardiac microlesion formation. Instruction is provided on microlesion visualization using microscopy, discrimination between early and late microlesions, and methods to detect cardiac remodeling in hearts of convalescent animals.
07:31
A Model of Cardiac Remodeling Through Constriction of the Abdominal Aorta in Rats
0 Views •
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.
06:55
Assessment of Maternal Vascular Remodeling During Pregnancy in the Mouse Uterus
0 Views •
Cited by 27 •
2015
This protocol describes a technique to assess changes in the maternal vasculature during pregnancy in mice. Using stereological methods, remodeling of the decidual spiral arteries is assessed quantitatively and the results confirmed qualitatively using immunohistochemistry.
11:10
Generation and Phenotypic Characterization of a CRISPR/Cas9-Engineered Cracd-Deficient Mouse Model for Post-Myocardial Infarction Remodeling Studies
0 Views •
2026
This protocol describes the generation and phenotypic characterization of a C57BL/6N-Cracdem1(c.538-83 to c.3352+255 del) mouse model using CRISPR/Cas9 technology to study the role of CRACD in cardiac remodeling following myocardial infarction.
02:54
Nucleosome Remodeling
0 Views •
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...
FAQs
The initiating stress shapes the remodeling pattern. Pressure or volume overload changes cardiac workload, whereas ischemia introduces injury-related signaling; both can promote cardiomyocyte hypertrophy, extracellular matrix deposition, fibrosis, inflammation, and altered ventricular function. Neurohormonal signaling provides another regulatory pathway that can influence these responses. Comparing these triggers helps researchers distinguish shared remodeling features from stimulus-specific adaptations.
Cardiomyocyte hypertrophy and extracellular matrix changes represent complementary parts of the remodeling response. Enlarged cardiomyocytes reflect cellular adaptation, while matrix deposition and fibrosis indicate structural changes in the tissue surrounding those cells. Inflammation adds another layer of response. Evaluating these features together allows researchers to relate cellular and tissue-level alterations to changes in ventricular function rather than treating remodeling as a single process.
Neurohormonal signaling can act as a regulatory driver of remodeling alongside mechanical stress and ischemic injury. Its influence may contribute to cardiomyocyte hypertrophy, extracellular matrix deposition, fibrosis, inflammation, or functional change. Including this pathway in experimental analysis helps researchers examine how signaling processes interact with altered workload and injury, supporting investigation of mechanisms relevant to heart failure.
A typical investigation combines a model that produces cardiac stress with measurements at multiple biological levels. Researchers may use genetic models or surgical interventions to create relevant conditions, then apply imaging to assess the heart and tissue analysis to examine structural changes. Tracking these measurements over time connects the initiating condition with molecular, tissue, and whole-organ outcomes.
Imaging helps researchers follow changes in cardiac structure and ventricular function in the living animal, while tissue analysis examines features such as cardiomyocyte hypertrophy, extracellular matrix deposition, fibrosis, and inflammation. Used together, these approaches show how microscopic alterations relate to organ-level performance. This combined information strengthens interpretation of remodeling progression and treatment effects.
The model supports cardiovascular medicine by linking molecular and tissue changes with whole-organ outcomes. Researchers use it to clarify mechanisms associated with heart failure, evaluate therapeutic targets, and examine how different stresses produce cardiac adaptations. Genetic models, surgical interventions, imaging, and tissue analysis provide complementary evidence, allowing potential mechanisms or interventions to be studied across several levels of cardiac organization.