Health & Medicine
Making Old Muscles Young and Fighting Fit During Aging
Brooke Miller
First Posted: Sep 27, 2012 06:46 AM EDT
The crucial factor that is responsible for declining muscle repair during aging has been traced by an international team of scientists. They have also revealed how to arrest the process in the mice with the aid of a common drug.
The study basically focused on the stem cells that are found inside the muscle. The stem cells are responsible for repairing injury. They focused on the stem cells in order to find out why the ability of the muscles to regenerate declines with age.
A dormant reservoir of stem cells is present inside every muscle, ready to be activated by exercise and injury to repair any damage. When required these cells have the capacity to divide into hundreds of new muscle fibers that repair the muscle. At the end of the repairing process certain cells replenish the dormant stem cells so that the muscle retains the ability to repair itself again and again.
The researchers had conducted the study on the old mice and found the number of dormant stem cells present in the pool reduces with age, which could explain the decline in the muscle's ability to repair and regenerate as it gets older.
The team screened these old muscles and noticed high levels of a protein known as FGF2 that has the ability to stimulate cells to divide.
As the process of the stem cells to divide and repair muscle is a normal and crucial process, they also observed that FGF2 has the capacity to awaken the dormant pool of stem cells even when they were not needed. The repeated activation of dormant cells indicates the pool was exhausted over time, so when the muscle really needed stem cells to repair itself the muscle was unable to respond properly.
Simultaneously the researchers also attempted to inhibit FGF2 in old muscles in order to prevent the stem cell pool from being activated into unnecessary action. On administering the common FGF2 inhibitor drug they were able to slow down the decline in the number of muscle stem cells in the mice.
The details of the study will be published in the journal Nature and was conducted by researchers from King's College London, Harvard University and Massachusetts General Hospital.
Dr Albert Basson, Senior Lecturer at the King's College London Dental Institute, said: 'Preventing or reversing muscle wasting in old age in humans is still a way off, but this study has for the first time revealed a process which could be responsible for age-related muscle wasting, which is extremely exciting.
'The finding opens up the possibility that one day we could develop treatments to make old muscles young again. If we could do this, we may be able to enable people to live more mobile, independent lives as they age.'
Dr Andrew Brack, senior and corresponding author of the study from Harvard University, said: 'Analogous to the importance of recovery for athletes training for a sporting event, we now know that it is essential for adult stem cells to rest between bouts of expenditure. Preventing stem cell recuperation leads to their eventual demise.'
Kieran Jones, co-author of the study from King's, added: 'We do not yet know how or why levels of the protein FGF2 increase with age, triggering stem cells to be activated when they are not needed. This is something that needs to be explored.
'The next step is to analyze old muscle in humans to see if the same mechanism could be responsible for stem cell depletion in human muscle fibers, leading to loss of mass and wastage.'
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First Posted: Sep 27, 2012 06:46 AM EDT
The crucial factor that is responsible for declining muscle repair during aging has been traced by an international team of scientists. They have also revealed how to arrest the process in the mice with the aid of a common drug.
The study basically focused on the stem cells that are found inside the muscle. The stem cells are responsible for repairing injury. They focused on the stem cells in order to find out why the ability of the muscles to regenerate declines with age.
A dormant reservoir of stem cells is present inside every muscle, ready to be activated by exercise and injury to repair any damage. When required these cells have the capacity to divide into hundreds of new muscle fibers that repair the muscle. At the end of the repairing process certain cells replenish the dormant stem cells so that the muscle retains the ability to repair itself again and again.
The researchers had conducted the study on the old mice and found the number of dormant stem cells present in the pool reduces with age, which could explain the decline in the muscle's ability to repair and regenerate as it gets older.
The team screened these old muscles and noticed high levels of a protein known as FGF2 that has the ability to stimulate cells to divide.
As the process of the stem cells to divide and repair muscle is a normal and crucial process, they also observed that FGF2 has the capacity to awaken the dormant pool of stem cells even when they were not needed. The repeated activation of dormant cells indicates the pool was exhausted over time, so when the muscle really needed stem cells to repair itself the muscle was unable to respond properly.
Simultaneously the researchers also attempted to inhibit FGF2 in old muscles in order to prevent the stem cell pool from being activated into unnecessary action. On administering the common FGF2 inhibitor drug they were able to slow down the decline in the number of muscle stem cells in the mice.
The details of the study will be published in the journal Nature and was conducted by researchers from King's College London, Harvard University and Massachusetts General Hospital.
Dr Albert Basson, Senior Lecturer at the King's College London Dental Institute, said: 'Preventing or reversing muscle wasting in old age in humans is still a way off, but this study has for the first time revealed a process which could be responsible for age-related muscle wasting, which is extremely exciting.
'The finding opens up the possibility that one day we could develop treatments to make old muscles young again. If we could do this, we may be able to enable people to live more mobile, independent lives as they age.'
Dr Andrew Brack, senior and corresponding author of the study from Harvard University, said: 'Analogous to the importance of recovery for athletes training for a sporting event, we now know that it is essential for adult stem cells to rest between bouts of expenditure. Preventing stem cell recuperation leads to their eventual demise.'
Kieran Jones, co-author of the study from King's, added: 'We do not yet know how or why levels of the protein FGF2 increase with age, triggering stem cells to be activated when they are not needed. This is something that needs to be explored.
'The next step is to analyze old muscle in humans to see if the same mechanism could be responsible for stem cell depletion in human muscle fibers, leading to loss of mass and wastage.'
See Now: NASA's Juno Spacecraft's Rendezvous With Jupiter's Mammoth Cyclone