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Updated: Aug 9, 2026

Detection and Isolation of Apoptotic Bodies to High Purity
Published on: August 12, 2018
Morphological aspects of apoptosis in heart diseases
Genzou Takemura1, Hisayoshi Fujiwara
1Second Department of Internal Medicine, Gifu University School of Medicine, Yanagido, Gifu, Japan.
Insights
Apoptosis plays a role in heart disease, but its direct evidence in cardiomyocytes is limited. Targeting apoptosis in non-myocytes shows promise for treating heart failure after myocardial infarction.
Area of Science:
- Cardiology
- Cell Biology
- Pathology
Background:
- Apoptosis (programmed cell death) is implicated in cardiomyocyte loss during myocardial infarction and heart failure.
- While experimental models show cardiomyocyte apoptosis, direct morphological evidence in human heart disease is scarce.
- Indirect evidence, like DNA fragmentation, suggests apoptosis occurs, but its clinical relevance remains debated.
Purpose of the Study:
- To critically review evidence on cardiomyocyte apoptosis in myocardial infarction and heart failure.
- To assess the role of apoptosis in non-myocyte interstitial cells in cardiac remodeling.
- To evaluate the therapeutic potential of targeting apoptosis in heart disease.
Main Methods:
- Systematic review of animal and human studies.
- Analysis of morphological, biochemical, and genetic data related to apoptosis.
- Evaluation of studies investigating therapeutic interventions targeting apoptosis.
Main Results:
- Limited direct morphological evidence of cardiomyocyte apoptosis in myocardial infarction and heart failure.
- Apoptosis is definitively observed in non-myocyte interstitial cells post-infarction.
- Blocking apoptosis in non-myocytes may mitigate cardiac remodeling and heart failure.
Conclusions:
- The precise role and clinical significance of cardiomyocyte apoptosis in heart disease require further elucidation.
- Non-myocyte apoptosis is a significant factor in post-infarction cardiac remodeling.
- Targeting non-myocyte apoptosis presents a potential therapeutic strategy for heart failure, but clinical application faces challenges.
Abstract:
It has been suggested that apoptosis may be responsible for a significant amount of cardiomyocyte death during acute myocardial infarction as well as for a progressive loss of surviving cells in failing hearts. Typical apoptosis can indeed be induced in cardiomyocytes at the experimental conditions. In actual heart diseases, in contrast, there is very little direct morphological evidence of apoptosis in cardiomyocytes occurring at any stage of myocardial infarction and heart failure, despite the availability of much indirect evidence that includes detection of DNA fragmentation and apoptosis-related factors. For that reason, the potential efficacy of therapeutic intervention to prevent apoptosis remains controversial. This review will survey available data from both animals and humans to critically assess the role of cardiomyocyte apoptosis during myocardial infarction and its relevance to myocardial remodeling and during progression to heart failure. Also considered will be nonmyocyte interstitial cells, which have received less attention than myocytes despite definitive evidence of their apoptosis in the infarcted heart and recent studies suggesting that blockade of apoptosis among these cells mitigates postinfarction cardiac remodeling and heart failure. We conclude from our survey that there are many hurdles to surmount before regulation of apoptosis can be clinically applied in the treatment of myocardial infarction and heart failure.
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