New discovery in stem cells may help build strong muscles in old age
The mutations occur during natural cell division, and the regions that are protected are those that are important for the function or survival of the cells. Nonetheless, the researchers were able to identify that this protection declines with age.Updated: Feb 25, 2018 16:41 IST
Researchers have found how an unexpectedly high number of mutations in the stem cells of muscles impair cell regeneration. As we grow older, our muscular function declines. So, according to the researchers, this discovery may result in new medication to build stronger muscles even when in old age.
For the study, published in the journal Nature Communications, researchers investigated the number of mutations that accumulate in the muscle’s stem cells (satellite cells).
“What is most surprising is the high number of mutations. We have seen how a healthy 70-year-old has accumulated more than 1,000 mutations in each stem cell in the muscle, and that these mutations are not random but there are certain regions that are better protected,” said co-author Maria Eriksson, professor at Sweden’s Karolinska Institutet.
The mutations occur during natural cell division, and the regions that are protected are those that are important for the function or survival of the cells. Nonetheless, the researchers were able to identify that this protection declines with age.
“We can demonstrate that this protection diminishes the older you become, indicating an impairment in the cell’s capacity to repair their DNA. And this is something we should be able to influence with new drugs,” said Eriksson.
The study was performed using single stem cells cultivated to provide sufficient DNA for whole genome sequencing.
“We achieved this in the skeletal muscle tissue, which is absolutely unique. We have also found that there is very little overlap of mutations, despite the cells being located close to each other, representing an extremely complex mutational burden,” the researcher noted.
First Published: Feb 25, 2018 16:39 IST