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Updated: Aug 15, 2026

Isolation and Functional Characterization of Human Ventricular Cardiomyocytes from Fresh Surgical Samples
Published on: April 21, 2014
[Death by apoptosis of cardiomyocytes: from the cells to clinics]
1INSERM Unité 460, Faculté de Médecine Xavier Bichat, Paris.
Insights
Heart disease involves changes in cardiomyocyte cell mass, with apoptosis (programmed cell death) emerging as a significant factor. Further research is needed to establish apoptosis
Area of Science:
- Cardiology and molecular biology
- Cardiac pathophysiology
- Cellular biology
Context:
- Myocardial remodeling in heart disease involves cellular changes like hypertrophy and altered protein activity.
- The regulation of cardiomyocyte cell mass in heart disease remains poorly understood.
- While cardiomyocyte hyperplasia is debated, a decrease in cell number may contribute to pathological changes.
Purpose:
- To review the role of cell loss, specifically apoptosis, in the context of heart disease.
- To highlight the growing evidence of cardiomyocyte apoptosis across various cardiomyopathies.
- To underscore the need for establishing the precise significance of apoptosis in heart disease pathophysiology.
Summary:
- Cellular processes such as hypertrophy and altered gene/protein activity are implicated in myocardial remodeling.
- A decrease in cardiomyocyte number, potentially through apoptosis, is increasingly recognized in conditions like ischemic, hypertrophic, and dilated cardiomyopathies.
- Apoptosis is a prominent topic in cardiology research but its exact role in heart disease pathogenesis requires further elucidation.
Impact:
- Establishes apoptosis as a key area of investigation in cardiovascular disease.
- Provides a foundation for future research into the mechanisms and therapeutic targeting of cardiomyocyte apoptosis.
- Emphasizes the need to bridge the gap between the prevalence of apoptosis research and its established clinical significance in heart failure.
Abstract:
Cell hypertrophy, modulations of gene expression or changes of the activity of proteins are known to play a role in remodelling of diseased myocardium. However, few data are available concerning regulation of the cell mass in heart disease. While cardiomyocyte hyperplasia remains controversial and probably constitutes a negligible phenomenon, the decreased number of cells could arguably contribute to alterations of the pathological myocardium. This loss of myocytes was mainly attributed to process of cell necrosis until it was demonstrated that cardiac myocytes can also die via apoptosis. This has been observed in ischaemic [1], hypertrophic [2], and dilated [3, 4] cardiomyopathy and in arrhythmogenic right ventricular dysplasia [5], to mention only the main diseases, and this list continues to grow [6]. Apoptosis therefore constitutes a major biological phenomenon in cardiology, at least at congresses and in scientific publications, but its place and significance in the pathophysiology of heart disease has yet to be established.
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