The article reviews the interplay between reactive oxygen species (ROS) and mitochondria in the context of aging and age-related diseases. It highlights the role of ROS in causing oxidative damage to mitochondrial DNA (mtDNA) and proteins, leading to mitochondrial dysfunction and increased ROS production in a vicious cycle. The authors discuss the free radical theory of aging, which posits that the accumulation of oxidative damage is a major cause of aging. They also explore the impact of ROS on cellular signaling, senescence, and stem cell aging, emphasizing the importance of ROS in maintaining tissue homeostasis and preventing degenerative diseases. Additionally, the article examines the mitochondrial theory of aging, focusing on the role of mtDNA mutations and oxidative stress in age-related neurodegenerative diseases such as Alzheimer's, Parkinson's, and Huntington's diseases. Finally, it reviews mouse models that have been used to study the relationship between oxidative stress, mitochondrial dysfunction, and aging, providing insights into potential therapeutic approaches for preventing or ameliorating age-associated degenerative diseases.The article reviews the interplay between reactive oxygen species (ROS) and mitochondria in the context of aging and age-related diseases. It highlights the role of ROS in causing oxidative damage to mitochondrial DNA (mtDNA) and proteins, leading to mitochondrial dysfunction and increased ROS production in a vicious cycle. The authors discuss the free radical theory of aging, which posits that the accumulation of oxidative damage is a major cause of aging. They also explore the impact of ROS on cellular signaling, senescence, and stem cell aging, emphasizing the importance of ROS in maintaining tissue homeostasis and preventing degenerative diseases. Additionally, the article examines the mitochondrial theory of aging, focusing on the role of mtDNA mutations and oxidative stress in age-related neurodegenerative diseases such as Alzheimer's, Parkinson's, and Huntington's diseases. Finally, it reviews mouse models that have been used to study the relationship between oxidative stress, mitochondrial dysfunction, and aging, providing insights into potential therapeutic approaches for preventing or ameliorating age-associated degenerative diseases.