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The Myocardial Unfolded Protein Response during Ischemic Cardiovascular Disease
1Department of Pathology and Feinberg Cardiovascular Research Institute, Feinberg School of Medicine, Northwestern University, 300 East Superior Street, Tarry Building 3-705, Chicago, IL 60611, USA.
Insights
Heart failure is rising, especially in the elderly. Targeting the unfolded protein response (UPR) in the heart may prevent cell death and slow disease progression after ischemic injury.
Area of Science:
- Cardiology
- Molecular Biology
- Cellular Biology
Background:
- Heart failure is a growing public health concern, particularly in aging populations.
- Ischemia, often resulting from atherosclerosis and myocardial infarction, is a primary driver of heart failure.
- Myocardial ischemic injury triggers the unfolded protein response (UPR) in cardiomyocytes, linked to cell death.
Purpose of the Study:
- To explore the connection between ischemia, the unfolded protein response (UPR), and cardiomyocyte cell death.
- To investigate the UPR's role in the pathogenesis of heart failure following ischemic events.
Main Methods:
- Review of recent studies on myocardial ischemic injury and the UPR.
- Analysis of the mechanisms linking ischemia, UPR activation, and apoptosis in cardiomyocytes.
Main Results:
- Myocardial ischemic injury activates the UPR in cardiomyocytes.
- UPR activation is associated with increased cardiomyocyte apoptosis and adverse cardiac remodeling.
- This cellular response contributes to the progression of heart failure post-myocardial infarction.
Conclusions:
- The unfolded protein response (UPR) plays a significant role in myocyte cell loss after ischemic injury.
- Targeting the myocardial UPR presents a potential therapeutic strategy for preventing heart failure progression.
- Intervention in the UPR pathway could mitigate adverse cardiac remodeling and preserve cardiac function.
Abstract:
Heart failure is a progressive and disabling disease. The incidence of heart failure is also on the rise, particularly in the elderly of industrialized societies. This is in part due to an increased ageing population, whom initially benefits from improved, and life-extending cardiovascular therapy, yet ultimately succumb to myocardial failure. A major cause of heart failure is ischemia secondary to the sequence of events that is dyslipidemia, atherosclerosis, and myocardial infarction. In the case of heart failure postmyocardial infarction, ischemia can lead to myocardial cell death by both necrosis and apoptosis. The extent of myocyte death postinfarction is associated with adverse cardiac remodeling that can contribute to progressive heart chamber dilation, ventricular wall thinning, and the onset of loss of cardiac function. In cardiomyocytes, recent studies indicate that myocardial ischemic injury activates the unfolded protein stress response (UPR) and this is associated with increased apoptosis. This paper focuses on the intersection of ischemia, the UPR, and cell death in cardiomyocytes. Targeting of the myocardial UPR may prove to be a viable target for the prevention of myocyte cell loss and the progression of heart failure due to ischemic injury.
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