Oxidative stress theory of aging. An imbalance between the antioxidant system and oxidants inevitably leads to oxidative stress, resulting in damage to cellular structures and macromolecules such as proteins, lipids, and DNA. This oxidative damage disrupts normal cellular functions and is intrinsically linked to various age-associated pathologies, including neurodegenerative diseases, cardiovascular disorders, and cancer. The accumulation of oxidative damage over time can trigger inflammatory responses, further exacerbating tissue injury and contributing to the aging process. Moreover, this imbalance can impair the body's ability to repair damaged molecules, resulting in a decline in cellular integrity and function. Cys:CySS, cysteine (Cys)/cystine (CySS); GSH:GSSG, reduced glutathione (GSH):oxidized glutathione (GSSG); SOD, superoxide dismutase; TrxSH:TrxSS, reduced and oxidised thioredoxin; UV, ultra violet.

Oxidative stress results from an imbalance between the production and neutralization of reactive oxygen species. It induces oxidative damage to cellular components including proteins, lipids, nucleic acids, and membranes, therefore intrinsically linking to aging-related diseases such as cancer, cardiovascular disease, and neurological disorders. Emerging evidence suggests that oxidative stress may promote tumor development by influencing various aspects of cellular senescence, such as its onset, pro-inflammatory secretion, and alteration of cellular function and structure. Modulating oxidative stress to target cellular senescence offers a novel strategy for cancer prevention and treatment. However, a thorough grasp of the specific mechanisms at play is lacking. This review will present the association between oxidative stress and cellular senescence and their regulatory role in tumor progression and treatment, with emphasis on senescence-associated secretory phenotype, immunosenescence and therapy-induced senescence. Current agents and strategies that remove side effects of cellular senescence via killing senescent cancer cells or modulating oxidative stress to improve antitumor efficacy will be summarized. This review will help readers better understand the complex relationship between oxidative stress and senescence in cancer, and will also provide a basis for further research in this area.

Article Access: https://doi.org/10.1002/mog2.70007

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