Key result
Inducing very low myocyte apoptosis causes lethal dilated cardiomyopathy in mice.
Why the study?
The pathogenesis of heart failure is poorly understood, and the causal role of low levels of cardiac myocyte apoptosis in heart failure remains unclear.
Does myocyte apoptosis cause heart failure, and does its inhibition prevent cardiac dilation and contractile dysfunction in a transgenic mouse model?
Population
Transgenic mice expressing a conditionally active caspase exclusively in the myocardium
Comparison
Induction of very low levels of myocyte apoptosis vs control mice with normal apoptosis levels
Design
Preclinical mechanistic study using transgenic mice
Authors
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Apoptosis inhibition merits study as a heart failure target; leaves open translation from transgenic mice to patients.
Does myocyte apoptosis cause heart failure, and does its inhibition prevent cardiac dilation and contractile dysfunction in a transgenic mouse model?
This study provides direct evidence that very low levels of myocyte apoptosis can cause heart failure, suggesting apoptosis inhibition as a potential therapeutic target.
Wencker et al. (2003) studied Heart failure. Conditionally active caspase expression (induction of myocyte apoptosis) vs. Controls was evaluated on Development of lethal, dilated cardiomyopathy. Induction of very low levels of myocyte apoptosis (23 per 10^5 nuclei) in transgenic mice was sufficient to cause lethal, dilated cardiomyopathy.
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