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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 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.

In this study of Han Chinese women, the mitochondrial DNA N haplogroup was associated with a higher risk of late-onset systemic lupus erythematosus and its specific manifestations, such as skin impairment and neurological disturbances.

This review summarizes current literature associating mitochondrial dysfunction with dermatologic issues like skin aging, hair loss, and poor wound healing, noting potential benefits in targeting mitochondrial components for treatments.

This article discusses the relationship between mitochondrial DNA damage and atherosclerosis, suggesting that mtDNA damage may increase plaque vulnerability independent of reactive oxygen species, but reports no new clinical results.