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Antioxidant and redox-related pathways represent a broad network of molecular systems designed to maintain cellular redox homeostasis by neutralizing reactive oxygen species (ROS) and reactive nitrogen species (RNS) [3.2.1, 3.2.5]. Central to these pathways is the Nrf2-Keap1 signaling axis, which orchestrates the expression of numerous cytoprotective and antioxidant genes, including those for superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx) [3.2.2, 3.2.5]. While physiological levels of ROS are vital for signal transduction and immune defense, an imbalance favoring pro-oxidants leads to oxidative stress, causing damage to DNA, proteins, and lipids [3.2.1, 3.2.4]. This dysregulation is a hallmark of various pathologies, including cancer, neurodegenerative diseases like Alzheimer's, and cardiovascular disorders [3.1.1, 3.2.5]. Therapeutic strategies targeting these pathways include Nrf2 activators such as dimethyl fumarate and ROS scavengers like N-acetylcysteine, which aim to restore balance and mitigate tissue damage [3.1.5, 3.2.2]. However, clinical application is complicated by the risk of 'reductive stress' and the potential for antioxidants to inadvertently protect malignant cells from oxidative-stress-induced apoptosis [3.1.3, 3.2.3].
Modulation of redox-sensitive transcription factors (e.g., Nrf2 activation), direct scavenging of reactive oxygen species (ROS), and inhibition of ROS-generating enzymes such as NADPH oxidase (NOX).
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