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Recent studies have suggested that various mechanisms and molecular pathways link oxidative stress to the pathogenesis of AV: toll-like receptors, peroxisome proliferator-activated receptors, the innate immune system, and mechanistic target of rapamycin.[] An imbalance in the production of oxygen-derived prooxidants, also known as reactive oxygen species (ROS), and the cellular capacity of antioxidant defense is believed to lead to oxidative stress

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