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Mitochondrial quality control mechanisms as molecular targets in cardiac ageing
Anna Picca1, Robert T Mankowski2, Jonathon L Burman2,3
1Department of Geriatrics, Neuroscience and Orthopedics, Teaching Hospital "Agostino Gemelli", Catholic University of the Sacred Heart School of Medicine, Rome, Italy.
Insights
Aging hearts show dysfunction due to impaired mitochondrial quality control. This review explores how issues in proteostasis, biogenesis, dynamics, and autophagy contribute to cardiac senescence and potential therapeutic targets.
Area of Science:
- Cardiology and Gerontology
- Mitochondrial Biology and Aging
Background:
- Cardiovascular disease (CVD) is a leading global cause of death.
- Advancing age is a primary risk factor for CVD due to cumulative exposure to risk factors and age-related cardiovascular changes.
- The aging heart undergoes structural and functional alterations, particularly affecting cardiomyocyte function and mitochondrial metabolism.
Purpose of the Study:
- To review the mechanisms linking defective mitochondrial quality control to organelle dysfunction in cardiac aging.
- To identify molecular pathways for preventing and treating age-related heart dysfunction.
Main Methods:
- Review of current literature on mitochondrial function, quality control, and cardiac aging.
- Analysis of molecular pathways involved in proteostasis, biogenesis, dynamics, and autophagy in the aging myocardium.
Main Results:
- Mitochondrial dysfunction is a key factor in cardiac senescence.
- Defective mitochondrial quality control mechanisms (proteostasis, biogenesis, dynamics, autophagy) exacerbate organelle dysfunction in aging hearts.
- These defects are amplified by cellular senescence.
Conclusions:
- Mitochondrial dysfunction and impaired quality control are central to age-related cardiac decline.
- Targeting these molecular pathways offers potential therapeutic strategies for preventing and treating cardiac aging and dysfunction.
Abstract:
Cardiovascular disease is the leading cause of morbidity and mortality worldwide. Advancing age is a major risk factor for developing cardiovascular disease because of the lifelong exposure to cardiovascular risk factors and specific alterations affecting the heart and the vasculature during ageing. Indeed, the ageing heart is characterized by structural and functional changes that are caused by alterations in fundamental cardiomyocyte functions. In particular, the myocardium is heavily dependent on mitochondrial oxidative metabolism and is especially susceptible to mitochondrial dysfunction. Indeed, primary alterations in mitochondrial function, which are subsequently amplified by defective quality control mechanisms, are considered to be major contributing factors to cardiac senescence. In this Review, we discuss the mechanisms linking defective mitochondrial quality control mechanisms (that is, proteostasis, biogenesis, dynamics, and autophagy) to organelle dysfunction in the context of cardiac ageing. We also illustrate relevant molecular pathways that might be exploited for the prevention and treatment of age-related heart dysfunction.
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