Mitochondria play a central role in aging, with mitochondrial dysfunction linked to aging-related phenotypes. While the mitochondrial free radical theory of aging (MFRTA) posits that reactive oxygen species (ROS) cause oxidative damage, recent evidence challenges this model. Instead, mtDNA mutations and mitochondrial dysfunction are increasingly recognized as key drivers of aging. mtDNA mutations accumulate with age, often due to clonal expansion of replication errors rather than damage accumulation. These mutations can impair mitochondrial function, leading to reduced energy production and increased ROS, which may contribute to progeroid phenotypes. However, some studies suggest that mtDNA mutations may not always increase oxidative stress, indicating that other mechanisms, such as impaired insulin/IGF-1 signaling and the target of rapamycin (TOR) pathways, may also be involved in aging. Mitochondrial function declines with age, affecting energy production and cellular processes. Somatic mtDNA mutations are associated with aging, particularly in stem cells, and may contribute to premature aging. However, the exact role of mtDNA mutations in aging remains unclear. Additionally, while antioxidant supplementation has been studied, it does not consistently improve longevity or health in humans. Instead, dietary restriction (CR) and exercise may improve mitochondrial function and longevity through various signaling pathways. The role of mitochondria in aging is complex, involving multiple pathways and mechanisms, and further research is needed to fully understand their contributions to the aging process.Mitochondria play a central role in aging, with mitochondrial dysfunction linked to aging-related phenotypes. While the mitochondrial free radical theory of aging (MFRTA) posits that reactive oxygen species (ROS) cause oxidative damage, recent evidence challenges this model. Instead, mtDNA mutations and mitochondrial dysfunction are increasingly recognized as key drivers of aging. mtDNA mutations accumulate with age, often due to clonal expansion of replication errors rather than damage accumulation. These mutations can impair mitochondrial function, leading to reduced energy production and increased ROS, which may contribute to progeroid phenotypes. However, some studies suggest that mtDNA mutations may not always increase oxidative stress, indicating that other mechanisms, such as impaired insulin/IGF-1 signaling and the target of rapamycin (TOR) pathways, may also be involved in aging. Mitochondrial function declines with age, affecting energy production and cellular processes. Somatic mtDNA mutations are associated with aging, particularly in stem cells, and may contribute to premature aging. However, the exact role of mtDNA mutations in aging remains unclear. Additionally, while antioxidant supplementation has been studied, it does not consistently improve longevity or health in humans. Instead, dietary restriction (CR) and exercise may improve mitochondrial function and longevity through various signaling pathways. The role of mitochondria in aging is complex, involving multiple pathways and mechanisms, and further research is needed to fully understand their contributions to the aging process.