The article discusses the role of mitochondria in aging, highlighting recent evidence that challenges the traditional mitochondrial free radical theory of aging (MFRTA). While MFRTA posits that reactive oxygen species (ROS) produced by mitochondria cause oxidative damage and contribute to aging, new findings suggest that increased mtDNA mutations, particularly in somatic stem cells, may drive progeroid phenotypes without significantly increasing oxidative stress. The authors also explore other mechanisms, such as insulin/IGF-1 signaling and target of rapamycin (TOR) pathways, which regulate longevity and are linked to mitochondrial function. They emphasize the need for further research to understand how mtDNA mutations accumulate and their impact on aging, as well as the potential therapeutic strategies to improve mitochondrial function and delay age-related diseases.The article discusses the role of mitochondria in aging, highlighting recent evidence that challenges the traditional mitochondrial free radical theory of aging (MFRTA). While MFRTA posits that reactive oxygen species (ROS) produced by mitochondria cause oxidative damage and contribute to aging, new findings suggest that increased mtDNA mutations, particularly in somatic stem cells, may drive progeroid phenotypes without significantly increasing oxidative stress. The authors also explore other mechanisms, such as insulin/IGF-1 signaling and target of rapamycin (TOR) pathways, which regulate longevity and are linked to mitochondrial function. They emphasize the need for further research to understand how mtDNA mutations accumulate and their impact on aging, as well as the potential therapeutic strategies to improve mitochondrial function and delay age-related diseases.