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.
12:03
Myocardial Infarction and Functional Outcome Assessment in Pigs
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Cited by 51 •
2014
This protocol describes the porcine myocardial infarction (MI) model using a 90 min closed-chest coronary balloon occlusion of the left anterior descending artery (LAD), followed by reperfusion. Furthermore, the protocol for several outcome parameters, such as cardiac function, hemodynamics, microvascular resistance, and infarct size, are also presented.
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.