The aging heart and post-infarction left ventricular remodeling
Henry Shih1, Brian Lee, Randall J Lee
1Department of Medicine, Division of Cardiology, University of California San Francisco, San Francisco, California 94143, USA.
Insights
Aging impairs heart cell repair after heart attacks, increasing heart failure risk in older adults. Cellular changes like reduced autophagy and stem cell function worsen outcomes in the aged heart.
Area of Science:
- Cardiology
- Gerontology
- Cellular Biology
Background:
- Aging is a significant risk factor for heart failure, a leading global cause of death.
- Elderly patients face higher risks of myocardial infarction (MI) and subsequent heart failure compared to younger individuals.
- Cellular aging processes in cardiomyocytes contribute to poor cardiovascular disease outcomes.
Purpose of the Study:
- To review the cellular and molecular mechanisms of post-infarction remodeling in the aged heart.
- To connect cellular changes with clinical outcomes in elderly patients experiencing MI.
- To elucidate how aging impacts cardiomyocyte biology and cardiac function post-MI.
Main Methods:
- Review of existing literature on cellular and molecular aging.
- Analysis of age-related changes in cardiomyocyte signaling pathways.
- Examination of impaired autophagy and apoptosis in aged cardiomyocytes.
- Investigation of reduced cardiomyocyte renewal and stem cell function in the elderly.
Main Results:
- Increased cellular stress and altered signaling pathways in aged cardiomyocytes.
- Impaired autophagy due to metabolic waste accumulation, promoting apoptosis.
- Reduced cardiomyocyte division and stem cell function contribute to cardiac dysfunction.
- Aged hearts exhibit maladaptive remodeling responses to MI and stress.
Conclusions:
- Cellular aging profoundly impacts the heart's ability to recover from myocardial infarction.
- Impaired cellular repair mechanisms, including autophagy and regeneration, are key in aged hearts.
- Understanding these cellular changes is crucial for improving clinical outcomes in elderly patients with heart failure post-MI.
Abstract:
Aging is a risk factor for heart failure, which is a leading cause of death world-wide. Elderly patients are more likely than young patients to experience a myocardial infarction (MI) and are more likely to develop heart failure following MI. The poor clinical outcome of aging in cardiovascular disease is recapitulated on the cellular level. Increase in stress exposure and shifts in signaling pathways with age change the biology of cardiomyocytes. The progressive accumulation of metabolic waste and damaged organelles in cardiomyocytes blocks the intracellular recycling process of autophagy and increases the cell's propensity toward apoptosis. Additionally, the decreased cardiomyocyte renewal capacity in the elderly, due to reduction in cellular division and impaired stem cell function, leads to further cardiac dysfunction and maladaptive responses to disease or stress. We review the cellular and molecular aspects of post-infarction remodeling in the aged heart, and relate them to the clinical problem of post-infarction remodeling in elderly patients.
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