Abstract

Corrupted integrity of the mitochondrial genome (mtDNA) accompanied by a gradual decline of mitochondrial function is a hallmark of aging. The majority of people carry the detectable levels of mtDNA mutations in somatic tissues, and the burden of those mutations builds up considerably with age. Hence, the causative nature of the relationship between the mtDNA mutations and aging emerges, awaiting further rigorous testing. Although over several decades numerous studies have been conducted and many experimental models developed, the origin and a precise time of occurrence of mtDNA mutations in the course of aging remain controversial. Here, we review the possible sources of somatic mtDNA mutations in our cells, and the mechanism underlying their expansion during aging. We also discuss whether in light of currently available evidence the link between mtDNA mutations and aging is credible.

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