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Published on: July 22, 2013
Monoamine Oxidases, Oxidative Stress, and Altered Mitochondrial Dynamics in Cardiac Ageing
Damien Maggiorani1, Nicola Manzella1, Dale E Edmondson2
1Institut des Maladies Métaboliques et Cardiovasculaires, INSERM, Université de Toulouse, Toulouse, France.
Insights
Monoamine oxidases (MAOs) contribute to aging-related cardiovascular diseases by increasing reactive oxygen species (ROS). Targeting MAOs may prevent age-associated heart conditions.
Area of Science:
- Cardiovascular Science
- Gerontology
- Biochemistry
Background:
- Increased longevity has led to a higher prevalence of age-dependent cardiovascular diseases.
- Cellular senescence is implicated in the etiology of age-related pathologies.
- Reactive oxygen species (ROS) accelerate cardiac senescence.
Purpose of the Study:
- To review recent advances in the role of monoamine oxidases (MAOs) in cardiovascular disease.
- To explore MAOs as potential therapeutic targets for age-associated cardiovascular conditions.
Main Methods:
- Review of scientific literature on MAO-A and MAO-B in cardiac aging.
- Analysis of the link between MAO activity, ROS production, and cardiovascular disease.
- Examination of age-related changes in MAO expression in cardiac tissue.
Main Results:
- MAO-A and MAO-B expression increases significantly with age in the heart.
- MAOs contribute to cardiac senescence through ROS generation, specifically hydrogen peroxide.
- MAO activity is linked to the development of age-associated cardiovascular diseases.
Conclusions:
- MAOs play a critical role in the pathogenesis of age-related cardiovascular diseases.
- MAOs represent promising therapeutic targets for preventing and treating cardiovascular conditions associated with aging.
Abstract:
The advances in healthcare over the past several decades have resulted in populations now living longer. With this increase in longevity, a wider prevalence of cardiovascular diseases is more common and known to be a major factor in rising healthcare costs. A wealth of scientific evidence has implicated cell senescence as an important component in the etiology of these age-dependent pathologies. A number of studies indicate that an excess of reactive oxygen species (ROS) contributes to trigger and accelerate the cardiac senescence processes, and a new role of monoamine oxidases, MAO-A and MAO-B, is emerging in this context. These mitochondrial enzymes regulate the level of catecholamines and serotonin by catalyzing their oxidative deamination in the heart. MAOs' expression substantially increases with ageing (6-fold MAO-A in the heart and 4-fold MAO-B in neuronal tissue), and their involvement in cardiac diseases is supposedly related to the formation of ROS, via the hydrogen peroxide produced during the substrate degradation. Here, we will review the most recent advances in this field and describe why MAOs could be effective targets in order to prevent age-associated cardiovascular disease.
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