Good at Heart: Preserving Cardiac Metabolism during aging
Daniela Sorriento, Antonietta Franco, Maria Rosaria Rusciano
1Department of Medicine and Surgery, University of Salerno, Italy.
Insights
Aging causes heart problems like hypertrophy and failure. Mitochondria dysfunction is key, offering potential targets for anti-aging heart therapies.
Area of Science:
- Cardiology
- Gerontology
- Mitochondrial Biology
Background:
- Aging leads to cardiac modifications, increasing heart disease risk and chronic heart failure.
- Common age-related cardiac changes include left ventricular hypertrophy, diastolic dysfunction, and fibrosis.
- Cellular homeostasis and maintenance mechanisms are significantly impacted by aging.
Purpose of the Study:
- To review the central role of mitochondria in the aging process.
- To explore molecular players involved in age-related heart failure progression.
- To identify potential "anti-aging" therapeutic strategies for cardiac health.
Main Methods:
- Review of current scientific literature on aging and cardiac function.
- Analysis of studies focusing on mitochondrial function, oxidative stress, and quality control.
- Examination of molecular mechanisms underlying age-related heart failure.
Main Results:
- Mitochondrial oxidative stress, impaired energy production, and compromised quality control are critical in aging.
- These mitochondrial dysfunctions contribute significantly to age-related cardiac remodeling and failure.
- Emerging molecular targets show promise for "anti-aging" interventions in the heart.
Conclusions:
- Mitochondria play a pivotal role in cardiac aging and the development of heart failure.
- Targeting mitochondrial pathways presents a promising avenue for novel anti-aging cardiac therapies.
- Further research into these molecular players could lead to effective strategies to combat age-related heart disease.
Abstract:
The natural process of aging determinates several cardiac modifications with increased susceptibility to heart diseases and ultimately converging on development of chronic heart failure as final stage. These changes mainly include left ventricular hypertrophy, diastolic dysfunction, valvular degeneration, increased cardiac fibrosis, increased prevalence of atrial fibrillation, and decreased maximal exercise capacity, as demonstrated in several humans and animal models of aging. While different theories have been proposed to explain the natural process of aging, it is clear that most of the alterations affect mechanisms involved in cell homeostasis and maintenance. Latest research studies have in particular focused on role of mitochondrial oxidative stress, energy production and mitochondria quality control. This article reviews the central role played by this organelle in aging and the role of new molecular players involved into the progression toward heart failure and potentially susceptible of new "anti-aging" strategies.
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