Reactive oxygen species-related pathways and redox homeostasis (ROS/Redox pathways)

Reactive oxygen species (ROS)-related pathways and redox homeostasis encompass the integrated biochemical systems responsible for maintaining a balance between the production of reactive oxygen species and their neutralization by antioxidant defenses [4, 12]. ROS, including superoxide anions, hydrogen peroxide, and hydroxyl radicals, are generated as natural byproducts of mitochondrial metabolism and by specific enzymes like NADPH oxidases (NOX) [10, 11]. At low to moderate levels, these species function as essential signaling molecules that regulate cell growth, apoptosis, and the immune response [14, 15]. However, a disruption in redox homeostasis leads to oxidative stress, which causes cumulative damage to cellular macromolecules such as DNA, lipids, and proteins [3, 17]. This imbalance is critically linked to the pathogenesis of various conditions, including cancer, cardiovascular diseases, and neurodegenerative disorders like Alzheimer's and Parkinson's [4, 5, 12]. Pharmacological intervention in these pathways typically focuses on enhancing antioxidant capacity through Nrf2 activators or inhibiting ROS-generating enzymes to mitigate tissue damage and restore cellular health [1, 2, 10]. Conversely, in oncology, some therapies aim to intentionally increase ROS levels to trigger apoptosis in cancer cells that are already under high oxidative pressure [6, 9]. The complexity of these pathways necessitates a precision medicine approach, as broad antioxidant supplementation has often failed in clinical trials due to the dual role of ROS in physiology [12, 14].

Other names

Oxidative stress pathwaysRedox signalingAntioxidant defense systemROS homeostasisRedox metabolism

Modulation of redox balance through the activation of antioxidant transcription factors (e.g., Nrf2), inhibition of ROS-generating enzymes (e.g., NOX, Xanthine oxidase), or direct scavenging of reactive species.