Researchers hope to control a group of mitochondrial proteins that attack and damage other functional cell parts, which leads to age-related diseases

Thomas Nyström, study leader and a researcher in the Department of Cell and Molecular Biology at the University of Gothenburg, and a team of researchers, have discovered that a group of mitochondrial proteins may be responsible for age-related diseases.

Scientists have theorized that the mitochondria, which are the power stations of cells, are responsible for human aging. This theory comes from the fact that mitochondria not only produce the body's energy, but also create harmful byproducts. These byproducts are reactive oxyradicals, and they attack several other parts of the cell. When a cell is attacked, it could become permanently damaged, which forces it to discontinue the operation of important functions. In the theory's conclusion, the lack of certain functional cells over time causes the organism to age.  

Now, Nyström and his colleagues have found that these mitochondrial proteins, called MTC proteins, may play a crucial role in age regulation in humans. The proteins are traditionally apart of mitochondrial protein synthesis, but have other roles that impact genome stability.

"When a certain MTC protein is lacking in the cell, e.g. because of a mutation in the corresponding gene, the other MTC proteins appear to adopt a new function," said Nyström. "They then gain increased significance for the stabilization of the genome and for combating protein damage, which leads to increased lifespan. 

"These studies also show that this MTC-dependent regulation of the rate of aging uses the same signaling pathways that are activated in calorie restriction - something that extends the lifespan of many different organisms, including yeasts, mice and primates. Some of the MTC proteins identified in this study can also be found in the human cell, raising the obvious question of whether they play a similar role in the regulation of our own aging processes."

While previous studies have shown that mitochondrial dysfunctions in cells delay aging in worms, fungi and flies, Nyström hopes to confirm the same in humans by controlling the mitochondrial proteins, which affect the cell's ability to remove the harmful proteins.  

"It is possible that modulating the activity of the MTC proteins could enable us to improve the capacity of the cell to delay the onset of age-related diseases," said Nyström. "These include diseases related to instability of the genome, such as cancer, as well as those related to harmful proteins, such as Alzheimer's disease and Parkinson's disease. At the moment this is only speculation, and the precise mechanism underlying the role of the MTC proteins in the aging process is a fascinating question that remains to be answered."

This study was published in Molecular Cell.

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