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Updated: Jun 16, 2026
Isolation and Physiological Analysis of Mouse Cardiomyocytes
Published on: September 7, 2014
Cell death in the pathogenesis of heart disease: mechanisms and significance
Russell S Whelan1, Vladimir Kaplinskiy, Richard N Kitsis
1Wilf Family Cardiovascular Research Institute and the Departments of Medicine and Cell Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA.
Abstract:
Cell death was once viewed as unregulated. It is now clear that at least a portion of cell death is a regulated cell suicide process. This type of death can exhibit multiple morphologies. One of these, apoptosis, has long been recognized to be actively mediated, and many of its underlying mechanisms have been elucidated. Moreover, necrosis, the traditional example of unregulated cell death, is also regulated in some instances. Autophagy is usually a survival mechanism but can occur in association with cell death. Little is known, however, about how autophagic cells die. Apoptosis, necrosis, and autophagy occur in cardiac myocytes during myocardial infarction, ischemia/reperfusion, and heart failure. Pharmacological and genetic inhibition of apoptosis and necrosis lessens infarct size and improves cardiac function in these disorders. The roles of autophagy in ischemia/reperfusion and heart failure are unresolved. A better understanding of these processes and their interrelationships may allow for the development of novel therapies for the major heart syndromes.
Insights
Cell death, including apoptosis and necrosis, is a regulated process in the heart. Understanding cell death mechanisms like autophagy could lead to new therapies for heart conditions.
Area of Science:
- Cardiovascular Biology
- Cellular Biology
- Pathology
Background:
- Cell death was historically considered unregulated, but is now understood as a regulated process with diverse morphologies.
- Apoptosis is a well-characterized regulated cell death pathway, while necrosis is also increasingly recognized as regulated.
- Autophagy, typically a survival mechanism, can be associated with cell death, though its mechanisms remain unclear.
Purpose of the Study:
- To explore the roles and interrelationships of apoptosis, necrosis, and autophagy in cardiac cell death.
- To investigate the potential for novel therapeutic strategies targeting these cell death pathways in major heart syndromes.
Main Methods:
- Review of existing literature on cell death mechanisms in cardiac myocytes.
- Analysis of the involvement of apoptosis, necrosis, and autophagy in myocardial infarction, ischemia/reperfusion, and heart failure.
Main Results:
- Apoptosis and necrosis are actively mediated and play significant roles in cardiac pathologies.
- Inhibition of apoptosis and necrosis has shown promise in reducing infarct size and improving cardiac function.
- The precise role of autophagy in cardiac ischemia/reperfusion and heart failure requires further investigation.
Conclusions:
- Understanding the complex interplay of regulated cell death pathways, including apoptosis, necrosis, and autophagy, is crucial for developing effective cardiac therapies.
- Targeting specific cell death mechanisms offers potential for improved treatment of major heart syndromes.
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