Abstract
Senescence is related to the loss of cellular homeostasis and functions, which leads to a progressive decline in physiological ability and to aging-associated diseases. Since mitochondria are essential to energy supply, cell differentiation, cell cycle control, intracellular signaling and Ca2+ sequestration, fine-tuning mitochondrial activity appropriately, is a tightrope walk during aging. For instance, the mitochondrial oxidative phosphorylation (OXPHOS) ensures a supply of adenosine triphosphate (ATP), but is also the main source of potentially harmful levels of reactive oxygen species (ROS). Moreover, mitochondrial function is strongly linked to mitochondrial Ca2+ homeostasis and mitochondrial shape, which undergo various alterations during aging. Since mitochondria play such a critical role in an organism’s process of aging, they also offer promising targets for manipulation of senescent cellular functions. Accordingly, interventions delaying the onset of age-associated disorders involve the manipulation of mitochondrial function, including caloric restriction (CR) or exercise, as well as drugs, such as metformin, aspirin, and polyphenols. In this review, we discuss mitochondria’s role in and impact on cellular aging and their potential to serve as a target for therapeutic interventions against age-related cellular dysfunction.
Highlights
In a rapidly aging society, new treatment options for age-related disorders and diseases will be increasingly important [1,2]
Since mitochondrial activity changes in a biphasic manner during aging [3], the right interventions need to be set at the right time to successfully counteract age-associated cellular dysfunction instead of triggering it
This review provides a summary of present knowledge about mitochondria’s unique role in the process of aging and the development of age-related disorders and diseases
Summary
In a rapidly aging society, new treatment options for age-related disorders and diseases will be increasingly important [1,2]. Recent reports suggest that mitochondrial function is linked to age-associated biphasic alterations in metabolic activity, including an increase and afterwards progressive decrease in mitochondrial function [3]. Changes in mitochondrial dynamics in fusion and fission, as well as alterations in the mitochondrial membrane potential [15] have been reported to cause cellular dysfunctions during senescence [16]. Since mitochondrial activity changes in a biphasic manner during aging [3], the right interventions need to be set at the right time to successfully counteract age-associated cellular dysfunction instead of triggering it. The potential of mitochondria to serve as targets for therapeutic interventions against age-related diseases is highlighted
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