Redox control of senescence and age-related disease

Abstract

The signaling networks that drive the aging process, associated functional deterioration, and pathologies has captured the scientific community's attention for decades. While many theories exist to explain the aging process, the production of reactive oxygen species (ROS) provides a signaling link between engagement of cellular senescence and several age-associated pathologies. Cellular senescence has evolved to restrict tumor progression but the accompanying senescence-associated secretory phenotype (SASP) promotes pathogenic pathways. Here, we review known biological theories of aging and how ROS mechanistically control senescence and the aging process. We also describe the redox-regulated signaling networks controlling the SASP and its important role in driving age-related diseases. Finally, we discuss progress in designing therapeutic strategies that manipulate the cellular redox environment to restrict age-associated pathology.

Graphical abstract

Highlights

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  Cellular aging corresponds to a cumulative failure of repair mechanisms, that mitigate damage from oxidants.

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  Age-associated redox imbalance drives pathological pathways.

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  The precise redox triggers that control the senescence-associated secretory phenotype are yet to be elucidated.

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  ROS-sensitive signaling networks may be potential therapeutic targets in restricting age-related pathologies.