Mitochondrial Dysfunction and the Cause of Healthy Aging: Treatment and Therapeutic Intervention

Abstract

Mitochondrial dysfunction is a common mechanism of cellular aging and age-related disease and thus a valuable therapeutic target for healthy aging. In the present review, the contribution of mitochondrial dysfunction to aging and specifically the evaluation of existing therapies for maintaining mitochondrial function have been discussed. Recent research between the years 2020-2025 was also looked for to introduce new treatment methods like mitochondrial transplantation, NAD+ supplementation, sirtuin activation, and senolytic therapy. Literature indicates that cellular senescence is triggered by mitochondrial dysfunction by decreased ATP production, increased reactive oxygen species (ROS) production, and disrupted mitochondrial quality control machinery. Therapeutic strategies that include mitochondrial biogenesis, dynamics, and turnover activity are also showing promise in phase I/II clinical and preclinical trials. Notably, organ-specific patterns of mitochondrial dysfunction can be a justification for precision medicine strategies to maximize the therapeutic efficacy. The latest findings nudge towards multi-targeting therapy crossing cellular senescence and mitochondrial function pathways as the optimal strategy for healthy aging. Subsequent research should be targeted at development of individualized regimens of treatment based on patients' idiosyncratic patterns of mitochondrial dysfunction and long-term safety profiles of novel drugs.