Mitochondrial Dysfunction in Aging: Future Therapies and Precision Medicine Approaches

Abstract

Mitochondria are the primary energy hubs of cells and are critical for maintaining cellular functions. However, aging leads to a decline in mitochondrial efficiency. This decline is marked by increased reactive oxygen species, accumulation of mitochondrial DNA mutations, impaired oxidative phosphorylation, and breakdown of mitochondrial quality control systems. Such changes are associated with the development of neurodegenerative, cardiovascular, and metabolic diseases. Although much research has been done, the precise connection between mitochondrial dysfunction and aging remains unclear. Furthermore, current literature exhibits a lack of systematic organization regarding the mitochondria-targeted therapeutic interventions. This review systematically explores the mechanisms underlying mitochondrial deterioration during aging. Key focuses include impaired biogenesis, disrupted dynamics, dysregulated stress responses, and defective clearance of damaged mitochondria. Additionally, this review explores innovative therapeutic strategies for these mitochondrial problems, including a combination of nanodelivery systems, artificially intelligent drug-screening techniques, and cutting-edge tools, such as CRISPR/Cas9 gene editing. By integrating recent advances in mitochondrial biology, this review provides a comprehensive framework that bridges basic mechanisms with clinical applications. The insights presented here underscore the potential of precision mitochondrial medicine as a novel approach to combating age-related disorders, enhancing our capacity to address age-related diseases, and foster healthy aging.