Aging-related tissue degeneration can be caused by mitochondrial dysfunction in tissue stem cells, according to the research group led by Professor Anu Suomalainen Wartiovaara at the University of Helsinki. Stem cells are called the spare parts for tissues, as they maintain and repair tissues during life, whereas mitochondria are the cellular engine transforming the energy of nutrients to a form that cells can use. In this process they burn most of the inhaled oxygen. If this nutrient 'burning' is inefficient, the engine will produce exhaust fumes, oxygen radicals, which damage cellular structures, including the genome.
In 2004 and 2005 a research model was created in Sweden and USA, which accumulated a heavy load of mitochondrial genome defects. This led to symptoms of premature aging: thin skin, graying of hair, baldness, osteoporosis and anemia. Scientist Kati Ahlqvist in Professor Suomalainen Wartiovaara's group showed that these symptoms were partially explained by stem cell dysfunction. The number of stem cells did not reduce, but their function was modified: the progeny cells in blood and the nervous system were dysfunctional. The Finnish researchers also discovered 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," says Professor Suomalainen Wartiovaara. The Finnish research group and their collaborators at the Max Planck Institute for Biology of Aging, Karolinska Institutet and University of Wisconsin have published their findings on the mechanisms of aging-associated degeneration in the international journal Cell Metabolism.
Source: University of Helsinki