Disorders of mitochondrial function in tissue stem cells can lead to tissue degeneration associated with aging. A research team led by Professor Anu Suomalainen Wartiovaara at the University of Helsinki in Finland collaborated with researchers at the Max Planck Institute in Germany on aging biology, Karolinska Institutet in Sweden and the University of Wisconsin in the United States On January 4, 2012, he published a research paper on aging-related degradation mechanisms in the journal Cell Metabolism.
Stem cells are called spare parts of tissues because they can repair and repair tissues throughout their lives. They are pluripotent and can produce a variety of different cell types, such as blood cells, neurons and skin cells. Mitochondria are the engines of cells: they convert the energy of nutrients into the energy form that cells can use, in the process they burn most of the oxygen they ingest. If the combustion of this nutrient is inefficient, the mitochondrial engine will produce exhaust gas and oxygen free radicals, and the oxygen free radicals destroy the cell structure including the genome. Antioxidants can scavenge these free radicals.
In 2004 and 2005, Swedish and American researchers have constructed a research model that accumulates a large number of mitochondrial genome defects, resulting in premature aging symptoms: skin thinning, hair graying, baldness, osteoporosis, and anemia.
Professor Suomalainen Wartiovaara said, "This suggests that oxygen free radicals regulate stem cell function and that these stem cells are very vulnerable to mitochondrial dysfunction. These findings may also be important in understanding the mechanism of mitochondrial disease."
These results are a breakthrough in revealing the unexpected importance of energy metabolism in regulating stem cell function and tissue maintenance. These findings deepen people's understanding of aging-related degradation mechanisms.
In the current study, Kati Ahlqvist, a scientist in Professor Suomalainen Wartiovaara's research group, confirmed that these symptoms can be partially explained by stem cell dysfunction. The researchers also found that early antioxidant treatment can partially prevent these defects from occurring.
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