Reactive oxygen species play a key and paradoxical role in tumor progression biology. At physiological levels, ROS act as important signaling molecules that control growth, survival, and metabolism. This redox balance becomes disrupted in cancer, leading to chronically elevated ROS levels that further promote genetic instability, metabolic changes, angiogenesis, spread, and resistance to chemotherapy or radiotherapy. Under prolonged oxidative stress, tumor cells strengthen antioxidant defense systems to avoid lethal oxidative damage. Conventional antioxidant approaches have shown limited clinical success. Indiscriminate ROS scavenging can disrupt essential redox-dependent signaling pathways and may compromise the effectiveness of ROS-based anticancer therapies. Redox-modulating nanoplatforms have emerged as a promising alternative by enabling precise, context-dependent modulation of redox homeostasis rather than global ROS suppression. With their tunable physical qualities, catalytic redox activity, and tumor-targeting potential, redox-modulating nanoplatforms can serve as dynamic redox buffers that specifically respond to the oxidative, acidic, and hypoxic tumor microenvironment without damaging the normal cells. These nano-systems regulate redox-sensitive signaling pathways, control mitochondrial ROS production, and influence ferroptosis and tumor microenvironment dynamics. Collectively, these effects improve therapeutic efficacy while reducing systemic toxicity. This review highlights current progress in nano-antioxidant design, processes of redox regulation, medicinal uses, and translational hurdles, showing their possible role in precision redox-based cancer treatment.
Faridi et al. (Sun,) studied this question.