The scientists working at University of California have solved the mystery of aging muscles where the biochemical pathways led to aging of the cells.

They did so by manipulating the pathways and so they could turn back the clock on old human muscle restoring the ability to repair and rebuild at its own.

"Our study shows that the ability of old human muscle to be maintained and repaired by muscle stem cells can be restored to youthful vigour given the right mix of biochemical signals," said Professor Irina Conboy, head of the research team conducting the study.

She also said, "This provides promising new targets for forestalling the debilitating muscle atrophy that accompanies aging and perhaps other tissue degenerative disorders as well."

Previously the scientists had confirmed that, the adult stem cells do the rebuilding activity on getting instruction from the muscle cells. With the passage of time, the molecular signals from the muscle cells change, which prevent the tissue repair work. This regenerative activity can be controlled by giving appropriate signals.

The regenerative function in old stem cells can be revived given the appropriate biochemical signals.

The scientists also found the stem cell receptor called Notch, which cause growth of the cells. Those stem cells also have a receptor called TGF-beta, which can cause a chain reaction decelerating the growth of the cells.

The progressive decline of such Notch cells and increased levels of TGF-beta are the main reasons in blocking the rebuilding capacity of those stem cells.

Irina Conboy and her group found that aging in mice is associated in part with the progressive decline of Notch and increased levels of TGF-beta, ultimately blocking the stem cells'' capacity to effectively rebuild the body.

Mitogen-activated protein (MAP), Kinase was an important regulator of Notch activity useful for human muscle repair, and its inactivity in old tissue triggered aging.

This important finding has been published in the journal EMBO Molecular Medicine.