Oxidative stress and mitochondrial dysfunction are key factors in aging and age-related diseases. Reactive oxygen species (ROS) contribute to aging by causing oxidative damage to DNA, proteins, and lipids, leading to mitochondrial dysfunction and further ROS production. Mitochondria, as the primary source of ROS, are central to aging processes. The free radical theory of aging suggests that ROS accumulation causes cellular damage, while mitochondrial dysfunction exacerbates this process. Studies show that increased ROS levels are associated with aging, and antioxidant defenses play a critical role in mitigating this damage. However, the role of ROS in aging remains debated, with some studies indicating that increased antioxidant enzymes do not necessarily extend lifespan. ROS also contribute to cellular senescence and stem cell aging by causing DNA damage and impairing cellular function. Mitochondrial dysfunction is linked to various age-related diseases, including neurodegenerative disorders like Alzheimer's, Parkinson's, and Huntington's disease, as well as cancer. Mitochondrial DNA mutations and oxidative damage are common in these conditions, highlighting the importance of mitochondrial health in aging. Mouse models have been used to study the relationship between oxidative stress, mitochondrial dysfunction, and aging, revealing that mitochondrial defects can lead to accelerated aging and disease. Overall, understanding the interplay between ROS, mitochondrial function, and aging is crucial for developing therapeutic strategies to combat age-related diseases.Oxidative stress and mitochondrial dysfunction are key factors in aging and age-related diseases. Reactive oxygen species (ROS) contribute to aging by causing oxidative damage to DNA, proteins, and lipids, leading to mitochondrial dysfunction and further ROS production. Mitochondria, as the primary source of ROS, are central to aging processes. The free radical theory of aging suggests that ROS accumulation causes cellular damage, while mitochondrial dysfunction exacerbates this process. Studies show that increased ROS levels are associated with aging, and antioxidant defenses play a critical role in mitigating this damage. However, the role of ROS in aging remains debated, with some studies indicating that increased antioxidant enzymes do not necessarily extend lifespan. ROS also contribute to cellular senescence and stem cell aging by causing DNA damage and impairing cellular function. Mitochondrial dysfunction is linked to various age-related diseases, including neurodegenerative disorders like Alzheimer's, Parkinson's, and Huntington's disease, as well as cancer. Mitochondrial DNA mutations and oxidative damage are common in these conditions, highlighting the importance of mitochondrial health in aging. Mouse models have been used to study the relationship between oxidative stress, mitochondrial dysfunction, and aging, revealing that mitochondrial defects can lead to accelerated aging and disease. Overall, understanding the interplay between ROS, mitochondrial function, and aging is crucial for developing therapeutic strategies to combat age-related diseases.