Mitochondrial DNA mutation accumulation may not be a determining factor in aging

The human genome is broadly classified into the genome residing in the cell nucleus (nuclear DNA) and the genome residing in the mitochondria (mitochondrial DNA: mtDNA). Mitochondria are cell organelles that produce energy essential for life activities through oxidative phosphorylation (mitochondrial respiration), and mtDNA encodes a set of genes required for mitochondrial respiration.

Previous research has led to the widely accepted hypothesis that the accumulation of multiple mutations in mtDNA with aging induces a decline in mitochondrial respiratory function, resulting in the “mitochondrial theory of aging.” Nevertheless, whether the decrease in mitochondrial respiratory function is actually due to these accumulated mutations has not been definitively established.

In this study, researchers demonstrated that mitochondrial respiratory function is not impaired even when wild-type mice accumulated mtDNA mutations to the same extent as in premature aging model mice.

The findings are published in the journal Aging Cell.

These results suggest that the decline in mitochondrial respiratory function is not directly caused by mtDNA mutations alone. Furthermore, the results call for a reinvestigation of the “mitochondrial theory of aging.”

The research team will continue to explore how various mutations accumulated in mtDNA contribute to symptoms of premature aging, aiming to expand our understanding of the relationship between aging and mitochondrial dysfunction.

The human genome is broadly classified into the genome residing in the cell nucleus (nuclear DNA) and the genome residing in the mitochondria (mitochondrial DNA: mtDNA). Mitochondria are cell organelles that produce energy essential for life activities through oxidative phosphorylation (mitochondrial respiration), and mtDNA encodes a set of genes required for mitochondrial respiration.

Previous research has led to the widely accepted hypothesis that the accumulation of multiple mutations in mtDNA with aging induces a decline in mitochondrial respiratory function, resulting in the “mitochondrial theory of aging.” Nevertheless, whether the decrease in mitochondrial respiratory function is actually due to these accumulated mutations has not been definitively established.

In this study, researchers demonstrated that mitochondrial respiratory function is not impaired even when wild-type mice accumulated mtDNA mutations to the same extent as in premature aging model mice.

The findings are published in the journal Aging Cell.

These results suggest that the decline in mitochondrial respiratory function is not directly caused by mtDNA mutations alone. Furthermore, the results call for a reinvestigation of the “mitochondrial theory of aging.”

The research team will continue to explore how various mutations accumulated in mtDNA contribute to symptoms of premature aging, aiming to expand our understanding of the relationship between aging and mitochondrial dysfunction.