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Death begets failure in the heart
Roger S-Y Foo1, Kartik Mani, Richard N Kitsis
1Department of Medicine, Cardiovascular Research Center, Albert Einstein College of Medicine, Bronx, New York 10461, USA.
The Journal of Clinical Investigation
|March 15, 2005
Abstract:
Recently, low--but abnormal--rates of cardiomyocyte apoptosis have been observed in failing human hearts. Genetic and pharmacological studies suggest that this cell death is causally linked to heart failure in rodent models. Herein, we review these data and discuss potential therapeutic implications.
Insights
Abnormal cardiomyocyte apoptosis, a form of cell death, is linked to heart failure. Research in rodent models suggests this cell death plays a causal role, offering potential therapeutic targets for heart failure.
Area of Science:
- Cardiology
- Molecular Biology
- Pathology
Background:
- Recent observations indicate low, yet abnormal, rates of cardiomyocyte apoptosis in failing human hearts.
- Cardiomyocyte apoptosis has been implicated as a contributing factor in the progression of heart failure.
Purpose of the Study:
- To review existing data on the role of cardiomyocyte apoptosis in heart failure.
- To discuss the potential therapeutic implications of targeting cardiomyocyte apoptosis.
Main Methods:
- Review of genetic studies in rodent models.
- Review of pharmacological studies in rodent models.
- Synthesis of current evidence linking cardiomyocyte apoptosis to heart failure.
Main Results:
- Genetic and pharmacological studies in rodent models suggest a causal link between cardiomyocyte apoptosis and heart failure.
- These findings highlight the significance of cardiomyocyte cell death in the pathophysiology of heart failure.
Conclusions:
- Cardiomyocyte apoptosis is a relevant factor in heart failure, supported by evidence from genetic and pharmacological studies.
- Targeting cardiomyocyte apoptosis presents a potential therapeutic strategy for managing heart failure.
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