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This study found that treating mtDNA mutator mice with the antioxidant SkQ1 delayed aging traits and extended their lifespan, potentially by alleviating mitochondrial dysfunction caused by reactive oxygen species.

This study found that oxidative damage is present in the mitochondria of PolG mice, which exhibit premature aging-like phenotypes due to mitochondrial dysfunction.

This review discusses the role of mitochondrial dysfunction in the ageing process and reports that its significance compared to other factors in mammalian ageing remains uncertain.

In this study, bezafibrate treatment improved certain aging-like features in a mouse model with mitochondrial dysfunction, but did not enhance muscle function or lifespan.

This study found that transient mtDNA double strand breaks in mice accelerated aging in certain tissues through increased reactive oxygen species, independent of p21/p53 pathway mediation.