Cardiomyocyte Hypertrophy
Cardiomyocyte Hypertrophy - Related Videos
06:51
Isolation and Culture of Adult Mouse Cardiomyocytes for Cell Signaling and in vitro Cardiac Hypertrophy
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Cited by 74 •
2014
We describe a reliable method for isolation of adult mouse cardiomyocytes. This protocol yields a consistent result for the culture of functional adult cardiomyocytes from a variety of genetically modified mice.
08:10
Micropatterned Magneto-Rheological Elastomers to Drive Changes in Cardiomyocyte Alignment
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Cited by 1 •
2025
We present a dynamic and reversible stiffness assay platform fabricated using an ultra-soft silicone elastomer (polydimethylsiloxane, PDMS) with embedded iron particles. This novel assay is suitable for studying emergent time-dependent physical changes in cell phenotypes, including contact guidance. Here, we measure neonatal rat cardiomyocyte alignment upon matrix stiffening using magnetics.
10:18
Ascending Aortic Constriction in Rats for Creation of Pressure Overload Cardiac Hypertrophy Model
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Cited by 17 •
2014
We describe a stepwise procedure for creating pressure overload and left ventricular hypertrophy in Wistar rats by constriction of the ascending aorta using a small metallic clip. This model is extensively used for studying remodeling changes during cardiac hypertrophy and for identifying and evaluating strategies for regression of such changes.
08:03
Simultaneous Assessment of Cardiomyocyte DNA Synthesis and Ploidy: A Method to Assist Quantification of Cardiomyocyte Regeneration and Turnover
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Cited by 25 •
2016
Quantification of cardiomyocyte turnover is challenging. The protocol described here makes an important contribution to this challenge by enabling accurate and sensitive quantification of neo-cardiomyocyte nuclei generation and nuclei ploidy.
07:50
Isolation and Culture of Neonatal Mouse Cardiomyocytes
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Cited by 187 •
2013
Primary mouse cardiomyocyte cultures are one of the pivotal tools for the investigation of myofibrillar organization and function. The following protocol describes the isolation and culture of primary cardiomyocytes from neonatal mouse hearts. The resulting cardiomyocyte cultures may be subsequently used for a variety of biomechanical, biochemical and cell-biological assays.
FAQs
Pressure or volume overload places mechanical stress on heart muscle cells, activating neurohormonal signals and intracellular signaling pathways. These pathways increase protein synthesis and promote sarcomere assembly, allowing the cells to generate or tolerate greater workload. The response therefore reflects coordinated structural remodeling rather than cell division.
Early enlargement can help the heart manage increased workload, but persistent stimulation may produce maladaptive remodeling. As the response continues, the heart may relax less effectively and develop fibrosis, a buildup of connective tissue. These changes can compromise cardiac performance and increase vulnerability to heart failure and arrhythmias.
The enlargement occurs through increased protein production and sarcomere assembly within existing heart muscle cells, not through cell division. This distinction matters because the heart adapts by changing the size and internal organization of individual cells. Studying that process helps explain how cardiac structure changes under sustained pressure or volume overload.
Medical research examines this remodeling in hypertension, valvular disease, and genetic cardiomyopathies. Each condition can alter the workload or structural environment of the heart, making cellular enlargement clinically relevant. Comparing these settings helps investigators connect changes in cardiac structure with impaired relaxation, fibrosis, heart failure, and arrhythmia risk.
These studies can connect mechanical stress and signaling activity with increased protein synthesis, sarcomere assembly, and later structural deterioration. They help clarify when remodeling remains compensatory and when it becomes harmful. The resulting information supports interpretation of how altered cardiac structure may contribute to impaired relaxation, fibrosis, heart failure, or arrhythmias.
Investigating the signaling and structural changes associated with cardiomyocyte hypertrophy provides a basis for developing and evaluating treatments intended to limit pathological remodeling. Such work is relevant when cardiac disease involves hypertension, valvular disease, or genetic cardiomyopathies. Treatment assessment can therefore focus on whether harmful changes in structure and function are reduced.