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Antioxidant and free radical targets represent a broad functional class of molecules involved in maintaining cellular redox homeostasis and protecting against oxidative damage. This group includes primary antioxidant enzymes such as superoxide dismutase (SOD), catalase, and glutathione peroxidase, which catalyze the conversion of reactive oxygen species (ROS) into less harmful molecules (Ighodaro & Akinloye, 2018, DOI: 10.1016/j.ajme.2017.09.001). It also encompasses the master transcriptional regulator Nrf2 (Nuclear factor erythroid 2-related factor 2), which orchestrates the expression of a wide array of cytoprotective genes in response to oxidative stress (He et al., 2020, PMCID: PMC7355540). In pathological states like neurodegeneration, diabetes, and cardiovascular disease, the overproduction of ROS or the depletion of antioxidant defenses leads to oxidative stress, causing damage to DNA, proteins, and lipids. Therapeutic strategies targeting these systems include Nrf2 activators like dimethyl fumarate, used in multiple sclerosis, and direct scavengers like edaravone, used in amyotrophic lateral sclerosis (Linker et al., 2011, Brain). However, because ROS also serve as critical secondary messengers in signaling pathways for cell growth and immune function, pharmacological modulation must be precisely controlled to avoid interfering with essential physiological processes (Sies & Jones, 2020, DOI: 10.1038/s41580-020-0230-3).
Activation of the Nrf2-Keap1-ARE signaling pathway to induce antioxidant gene expression, direct chemical neutralization of reactive oxygen species, or inhibition of pro-oxidant enzymes like NADPH oxidase.
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