The nuanced role of mitochondrial ROS in modulating aging and aging hallmarks.
Abstract
Aging is characterized by a progressive decline in cellular integrity and function, making it a major risk factor for numerous disease pathologies. Mitochondrial dysfunction and oxidative stress have long been recognized as contributors to the aging phenotype. The loss of mitochondrial function and the overproduction of reactive oxygen species (ROS) are linked to many hallmarks of aging and are associated with a wide range of diseases; however, their role in the aging process is nuanced. Mitochondria produce ROS as harmful respiratory byproducts, but ROS can also act as a signaling molecule with emerging functions linked to variables such as location, timing, and quantity. Similarly, mitochondrial dysfunction is often broadly categorized, overlooking its multifaceted nature and diverse contributions to aging. Due to this complexity, our understanding of how mitochondrial ROS production shapes disease processes and aging hallmarks remains limited. This review aims to clarify the complex and nuanced role of mitochondrial ROS in aging by focusing on ROS production within mitochondria, especially complexes I, II and III, and exploring how these localized ROS influence various hallmarks of aging to contribute to the aging phenotype.
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Research summary
The paper posits that mitochondrial ROS acts as a context-dependent signaling molecule rather than solely a damaging byproduct, influencing specific aging hallmarks based on location and timing. This is a review article that synthesizes existing knowledge on the nuanced role of mitochondrial ROS in aging, providing a conceptual framework for understanding aging mechanisms but lacking the novel experimental data or breakthrough discoveries required for a higher impact score.
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