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Death by design. Programmed cell death in cardiovascular biology and disease
1Molecular Cardiology Unit, Baylor College of Medicine, Houston, Tex 77030, USA.
Abstract:
Programmed cell death (apoptosis) is recognized, increasingly, as a contributing cause of cardiac myocyte loss with ischemia/reperfusion injury, myocardial infarction, and long-standing heart failure. Although the exact mechanisms initiating apoptosis in these in vivo settings remain unproven, insights into the molecular circuitry controlling apoptosis more widely suggest the potential to protect mammalian ventricular muscle from apoptosis through one or more of these pathways, by pharmacological means or, conceivably, gene transfer.
Insights
Programmed cell death, or apoptosis, contributes to heart muscle cell loss in various heart conditions. Targeting apoptosis pathways may offer new ways to protect heart muscle from damage.
Area of Science:
- Cardiovascular Biology
- Cell Death Mechanisms
Background:
- Programmed cell death (apoptosis) is increasingly implicated in cardiac myocyte loss.
- This loss is observed in conditions such as ischemia/reperfusion injury, myocardial infarction, and chronic heart failure.
Purpose of the Study:
- To explore the role of apoptosis in cardiac myocyte loss.
- To identify potential therapeutic strategies for protecting heart muscle from apoptosis.
Main Methods:
- Review of existing literature on apoptosis mechanisms.
- Analysis of molecular circuitry controlling apoptosis in mammalian systems.
Main Results:
- Apoptosis is a significant factor in cardiac myocyte loss across several cardiovascular pathologies.
- The precise in vivo triggers for apoptosis in these settings require further elucidation.
Conclusions:
- Understanding apoptosis pathways offers potential for novel cardioprotective therapies.
- Pharmacological or gene transfer approaches targeting apoptosis may mitigate cardiac myocyte loss.