Mitochondrial dysfunction in cardiac aging
Autumn Tocchi1, Ellen K Quarles1, Nathan Basisty1
1University of Washington School of Medicine, Department of Pathology, Box 357470, Seattle, WA 98195-7470, USA.
Insights
Aging significantly elevates cardiovascular disease risk by impairing cardiac function through mitochondrial dysfunction. This review explores these mitochondrial changes and potential targeted treatments for cardiac aging.
Area of Science:
- Cardiology
- Gerontology
- Mitochondrial Biology
Background:
- Cardiovascular diseases (CVDs) are a primary cause of mortality globally.
- Aging is the most significant risk factor for CVDs, with prevalence increasing sharply with age.
- Cardiac aging involves intrinsic functional, cellular, and molecular decline.
Purpose of the Study:
- To review the role of mitochondrial dysfunction in cardiac aging.
- To explore mechanisms maintaining mitochondrial homeostasis.
- To discuss emerging mitochondrial-targeted therapies for aging hearts.
Main Methods:
- Literature review of recent research on cardiac aging and mitochondria.
- Analysis of cellular and molecular changes associated with aging mitochondria.
- Examination of pathways involved in mitochondrial quality control.
Main Results:
- Mitochondrial dysfunction disrupts cardiac morphology, signaling, and protein interactions.
- Mechanisms like mitochondrial fission/fusion, autophagy, and unfolded protein responses maintain homeostasis.
- Impaired mitochondrial function is a key driver of cardiac aging.
Conclusions:
- Mitochondrial dysfunction is central to the pathophysiology of cardiac aging.
- Targeting mitochondrial pathways offers potential therapeutic strategies.
- Further research into mitochondrial treatments is crucial for addressing age-related cardiac decline.
Abstract:
Cardiovascular diseases are the leading cause of death in most developed nations. While it has received the least public attention, aging is the dominant risk factor for developing cardiovascular diseases, as the prevalence of cardiovascular diseases increases dramatically with increasing age. Cardiac aging is an intrinsic process that results in impaired cardiac function, along with cellular and molecular changes. Mitochondria play a great role in these processes, as cardiac function is an energetically demanding process. In this review, we examine mitochondrial dysfunction in cardiac aging. Recent research has demonstrated that mitochondrial dysfunction can disrupt morphology, signaling pathways, and protein interactions; conversely, mitochondrial homeostasis is maintained by mechanisms that include fission/fusion, autophagy, and unfolded protein responses. Finally, we describe some of the recent findings in mitochondrial targeted treatments to help meet the challenges of mitochondrial dysfunction in aging.
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