When we’re young, we bounce back from injury fairly quickly. As we age, we lose that capacity to rebuild our muscles and get back in the game.
The question is, why? New research into muscle stem cells is helping solve the puzzle.
Working with mice, a team led by Dr. Michael Rudnicki, senior scientist at the Ottawa Hospital Research Institute (OHRI), found that as muscle stem cells age, their functionality is compromised by increased activation of a signalling pathway called JAK/STAT that transmits information to cells from surrounding tissue.
“What’s really exciting to our team is that when we used specific drugs to inhibit the JAK/STAT pathway, the muscle stem cells in old animals behaved the same as those found in young animals,” Dr. Rudnicki, who is a member of our Foundation’s Board of Directors, explained in an OHRI media release. “These inhibitors increased the older animals’ ability to repair injured muscle and to build new tissue.”
The findings were published last week in the prestigious journal Nature Medicine.
According to the media release, the stem cells aren’t getting the message to maintain their populations. As we age, the JAK/STAT pathway gets busier, altering how muscle stem cells, called satellite cells, divide and reducing the number of regenerating cells. This, in turn, reduces our capacity to repair and rebuild muscle.
While this is early stage research, the implications are exciting. It opens up the possibility of developing JAK/STAT inhibiting drugs to treat muscle-wasting diseases such as muscular dystrophy.
The next step is looking for less toxic molecules — the drugs used in this study are commonly used for chemotherapy — that could have the same effect.
For more information about stem cells and muscular dystrophy, click here.