Tissue Degeneration Found In Aging Is Partially Caused By Mitochondrial Dysfunction In Stem Cells

Research models have preciously found that an accumulation of mitochondrial genome defects leads to symptoms of premature aging: thin skin, graying of hair, baldness, osteoporosis and anemia.

In a breakthrough revealing the unexpected importance of energy metabolism in regulating stem cell function and tissue maintenance, new research on the mechanisms of age-associated degeneration indicates that tissue degeneration can be caused by mitochondrial dysfunction in tissue stem cells. Stem cell function may be modified with the result that progeny cells in blood and the nervous system are dysfunctional.

Mitochondria are the cellular engine: they transform the energy of nutrients to a form that cells can use, and in this process they burn most of oxygen we inhale. If this nutrient 'burning' is inefficient, the engine will produce oxygen radicals that damage cellular structures, including the genome. The researchers also found that these defects could be partially prevented by early antioxidant treatment.

"This suggests that oxygen radicals can regulate stem cell function and that these cells are very susceptible for mitochondrial dysfunction. These findings may also be important to understand mechanisms of mitochondrial disease", said Professor Anu Suomalainen Wartiovaara of Helsinki University. His team collaborated in the research with researchers at Max Planck Institute for Biology of Aging, Karolinska Institute and the University of Wisconsin.

Adapted from the University of Helsinki announcement.