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As a metabolite of vitamin A, retinoic acid (RA) is bound to nuclear receptors (RAR/RXR) to produce effects and regulate gene expression, showing antioxidant, anti-inflammatory, and anti-apoptotic activities [1]. Oxidative stress, induced by both endogenous and exogenous factors, results in the excessive accumulation of reactive oxygen species (ROS) in specific areas, which can damage cellular components and lead to neurodegenerative diseases, cancer, cardiovascular diseases, and photoaging. RA modulates oxidative stress through various molecular mechanisms, including interaction with the Nuclear factor erythroid 2-related factor 2- Kelch-like ECH-associated protein 1 (Nrf2-Keap1) pathway and epigenetic regulation of antioxidant enzymes [2]. Research suggests that RA has considerable benefits in treating a range of diseases, including neurodegenerative diseases, skin aging, obesity, and metabolic syndrome. This review aims to provide an overview of the molecular mechanisms by which RA regulates oxidative stress and evaluate its therapeutic potential in these diseases, offering insights for future applications of RA in the prevention and treatment of these conditions.