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Role of apoptosis in cardiovascular disease
Youngil Lee1, Asa B Gustafsson
1BioScience Center, San Diego State University, San Diego, CA 92182-4650, USA.
Insights
Apoptosis, a regulated cell death, is crucial in cardiovascular diseases like heart failure. Inhibiting this process in cardiac myocytes offers cardioprotection and prevents disease progression.
Area of Science:
- Cardiovascular biology
- Cellular biology
- Pathophysiology
Background:
- Apoptosis, or programmed cell death, is implicated in cardiovascular diseases through the loss of cardiac myocytes.
- Cardiac myocyte apoptosis is observed in conditions such as myocardial infarction, diabetic cardiomyopathy, and heart failure.
- Cellular stressors like cytokines, oxidative stress, and DNA damage activate apoptosis in cardiac myocytes.
Purpose of the Study:
- To review the evidence linking apoptosis to cardiovascular diseases.
- To discuss the molecular pathways governing cardiac myocyte apoptosis.
Main Methods:
- Review of existing scientific literature on apoptosis in cardiovascular diseases.
- Analysis of molecular mechanisms driving cardiac myocyte apoptosis.
Main Results:
- Apoptosis is a significant factor in the pathogenesis of various cardiovascular diseases.
- Inhibition of apoptosis has demonstrated cardioprotective effects, preventing heart failure development.
Conclusions:
- Apoptosis is a critical cellular process in cardiovascular disease development.
- Targeting apoptosis pathways presents a potential therapeutic strategy for cardioprotection and heart failure prevention.
Abstract:
Apoptosis plays a key role in the pathogenesis in a variety of cardiovascular diseases due to loss of terminally differentiated cardiac myocytes. Cardiac myocytes undergoing apoptosis have been identified in tissue samples from patients suffering from myocardial infarction, diabetic cardiomyopathy, and end-stage congestive heart failure. Apoptosis is a highly regulated program of cell death and can be mediated by death receptors in the plasma membrane, as well as the mitochondria and the endoplasmic reticulum. The cell death program is activated in cardiac myocytes by various stressors including cytokines, increased oxidative stress and DNA damage. Many studies have demonstrated that inhibition of apoptosis is cardioprotective and can prevent the development of heart failure. This review provides a current overview of the evidence of apoptosis in cardiovascular diseases and discusses the molecular pathways involved in cardiac myocyte apoptosis.
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