Myocardial Remodeling
Myocardial Remodeling - Related Videos
11:10
Generation and Phenotypic Characterization of a CRISPR/Cas9-Engineered Cracd-Deficient Mouse Model for Post-Myocardial Infarction Remodeling Studies
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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
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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 29 •
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.
09:45
Histological Quantification of Chronic Myocardial Infarct in Rats
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Cited by 13 •
2016
The post-mortem assessment of myocardial infarction (MI) in rodents is based on quantification of the infarct on stained heart sections. We describe an accurate method to quantify the infarct size using systematic sampling of harvested rat hearts from base to apex and image analyses of trichrome-stained histological sections.
04:29
A Modified Simple Method for Induction of Myocardial Infarction in Mice
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Cited by 3 •
2021
Under adequate anesthesia, the mouse heart was externalized through the intercostal space, and myocardial infarction was successfully induced by ligating the left anterior descending artery (LAD) using materials readily available in most laboratories.
FAQs
Mechanical strain and neurohormonal signaling act as important drivers of the cardiac response. They can promote coordinated changes in cardiomyocytes, the extracellular matrix, and chamber structure rather than affecting a single component in isolation. Examining these signals helps distinguish remodeling associated with altered workload from changes occurring under chronic physiological stress.
Changes in the extracellular matrix are consequential because matrix turnover and fibrosis can alter the heart’s structural environment. When these processes occur alongside cardiomyocyte hypertrophy or chamber dilation, they may change cardiac performance. Considering the components together gives researchers a more complete way to interpret whether remodeling remains adaptive or becomes maladaptive.
Behavioral states can modify the conditions under which remodeling develops. Regular physical activity, prolonged inactivity, smoking, diet, and chronic stress are relevant variables, but they should not be treated as interchangeable exposures. Comparing these factors helps investigators connect modifiable behavior with the mechanical or physiological circumstances that may influence cardiac adaptation.
Remodeling becomes especially important when behavioral and physiological influences are considered together. A behavior may affect the workload or stress environment in which the myocardium adapts, while structural changes may influence cardiac performance. This combined context helps explain why behavior is relevant to heart-failure progression without reducing the process to a single lifestyle factor.
Researchers can relate behavioral states and lifestyle factors to changes in cardiomyocyte hypertrophy, extracellular-matrix turnover, fibrosis, and chamber dilation. They can then consider how those changes correspond with cardiac performance, heart-failure progression, or responses to treatment. This approach connects behavioral context with both structural adaptation and clinically relevant cardiac outcomes.
This research can identify modifiable behavioral and psychological factors associated with conditions that promote cardiac remodeling. Linking those factors with cardiac performance, heart-failure progression, and treatment response provides a scientific basis for prevention strategies. The goal is to address relevant risks while recognizing that remodeling reflects interactions among behavior, workload, stress, and myocardial adaptation.