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Mitochondrial Reactive Oxygen Species in Cellular Senescence

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Part of the book series: Healthy Ageing and Longevity ((HAL))

Abstract

Mitochondria are central for the maintenance of cellular homeostasis and both cellular dysfunction and aging are linked to mitochondrial dysfunction. Mitochondrial dysfunction is the principle cause of increased levels of reactive oxygen species (ROS) and oxidative stress, which is a key mediator of aging. The cell responds to this stressful stimulus by the induction of the cellular aging-stress response, cellular senescence. Here, we discuss the mechanisms through which mitochondrial ROS promotes senescence. In this context, we will highlight how mitochondrial ROS serves an initiating upstream, or sustaining downstream, role in the induction of senescence. We will also discuss potential interventions to alleviate mitochondrial ROS and delay cellular senescence.

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Correspondence to Christian Sell Ph.D. .

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Nacarelli, T., Torres, C., Sell, C. (2016). Mitochondrial Reactive Oxygen Species in Cellular Senescence. In: Rattan, S., Hayflick, L. (eds) Cellular Ageing and Replicative Senescence. Healthy Ageing and Longevity. Springer, Cham. https://doi.org/10.1007/978-3-319-26239-0_10

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