Every cell contains hundreds of mitochondria, actively generating adenosine triphosphate (ATP), a chemical energy store molecule used to power cell processes. Mitochondria are descended from symbiotic bacteria and retain many bacterial features, such as a circular genome, the mitochondrial DNA, and the ability to replicate and fuse together. Nonetheless, they have become cell components and are recycled by the quality control mechanism of mitophagy when damaged. In aged tissues, mitochondria become altered in size, activity, and ability to produce ATP for reasons that may have as much to do with epigenetic changes in the cell nucleus as they do with damage to mitochondrial DNA. It is thought that this mitochondrial dysfunction is an important contributing cause of degenerative aging.
Mitochondria are unique double-membrane organelles that came into existence due to the engulfment of alpha-proteobacterium by a eukaryotic progenitor cell in an endosymbiosis process, demonstrating evolutionary importance in the advancement of eukaryotic life. Mitochondria, apart from the nucleus, comprises its genome, metabolome, transcriptome, and proteome. Mitochondria have been considered a cellular powerhouse, responsible for approximately 95% of cellular ATP production. They are responsible for significantly contributing to the maintenance of cellular homeostasis by contributing to metabolic processes such as the tricarboxylic acid cycle (TCA) and oxidative phosphorylation (OXPHOS).
Apart from regulating cellular energetics, mitochondria also play an essential role in intracellular calcium signaling, thermogenesis, apoptosis, generation of reactive oxygen species (ROS), and regulation of oxidative stress response. Any defect or deficit in mitochondrial number and function might be responsible for cellular damage. Mitochondrial dysfunction has been reported to be associated with aging and almost all chronic aging-associated diseases through reduced ATP production, alteration in the regulation of apoptosis, increased ROS production, and defective calcium signaling.
Accumulation of mutations in mitochondrial DNA (mtDNA) is the primary cause of mitochondrial anomalies, further contributing to aging and associated diseases. Here, we provide a detailed description of mitochondrial dysfunction, its implications in the aging process, the onset of aging-associated diseases, and potential therapeutic interventions targeting mitochondrial dysfunction to develop an effective strategy for treating age-related diseases.
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