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Systematic review reveals how core redox pathways govern cell fate in animals, highlighting mechanistic networks linking oxidative distress to tissue damage and aging.
Oxidative stress is caused by the imbalance between the generation of free reactive oxygen species (ROS)/reactive nitrogen species (RNS) and the antioxidant defense systems, which participate in animal growth, development, disease pathogenesis, and aging. This review summarizes endogenous and exogenous triggers of ROS/RNS overproduction, as well as model animals and cell models together with oxidative stress biomarkers and detection methods. We further dissect the three-layered redox regulatory network, focusing on crosstalk among four core pathways (Nrf2-ARE, NF-κB, MAPK, PI3K/Akt) that govern cell fate via oxidative eustress or distress. Excessive ROS/RNS trigger irreversible DNA damage and metabolic disorders, leading to inflammation and apoptosis. Finally, we prospect integrating non-model animals and multi-omics to advance oxidative stress research. This work provides a comprehensive theoretical framework for animal redox biology studies.
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Chang et al. (2026) studied this question.
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