As cellular power centers, the main function of mitochondria is to produce ATP via the process of oxidative phosphorylation, which is carried out by the four respiratory chain complexes and ATP synthase located in the inner mitochondrial membrane (IMM). Other biochemical functions of mitochondria include the regulation of metabolic (both catabolic and anabolic), signaling pathways and apoptosis (Nunnari and Suomalainen, 2012). Mitochondria are unique cellular organelles that contain their own genetic information, the mitochondrial DNA (mtDNA), a double-stranded and circular molecule of 16.5 kb in size (Yue et al., 2015).
Emerging evidence has elucidated the precise relationship between mitochondrial function, and signaling pathways regulating lifespan and aging. During aging, decline in the number of mitochondrial, mtDNA copy number and protein levels of mitochondria were observed both in human and in mice (Bratic and Larsson, 2013). Damage in mtDNA with aging causes defects in the encoding proteins for the respiratory chain which in turn amplifies ROS production and mitochondrial dysfunction (Van Houten et al., 2006). Furthermore, this age-related progressive mitochondrial dysfunction results in further increased levels of ROS production causing severe mitochondrial deterioration and extensive cellular damage.
Accumulating evidence has shown mitochondrial dysfunction works in conjuction with several other aging hallmarks (including loss of proteostasis, cellular senescence, and stem cell exhaustion) to accelerate the aging process (Vermulst et al., 2008). Aggravated mitochondrial dysfunction and DNA are associated with a variety age-related human diseases, including cancer, diabetes and COPD (Ahmad et al., 2015; Boland et al., 2013; Montgomery and Turner, 2014; Rera et al., 2012). Therefore, improvement of mitochondrial function is potential therapeutic strategy to delay the onset of age-related diseases.