Muscle weakness can be reversed

A protein complex that helps the muscle
promotes growth, muscle
cause loss if it is
is very active; © panthermedia.net/
Joerg Michael Gehrke

The protein complex mTORC1 promotes muscle growth. However, if it is permanently active, it impairs the self-cleaning of cells and leads to muscle disease. Scientists at the University of Basel describe this mechanism.

As with a machine, individual components in the cell also wear out over time. In order for the cell to remain healthy, defective components and waste materials must be regularly disposed of or reprocessed. This is ensured by a cellular self-cleaning process - autophagy.

However, the capacity for self-renewal decreases with age. This creates a multitude of age-related diseases such as cancer, heart disease and muscle weakness. The growth regulator mTORC1 plays a major role in this. The team headed by Professor Markus Rüegg from the Biozentrum of the University of Basel and researchers from the Department of Biomedicine have now discovered the exact connection.

Until now it was assumed that the protein complex mTORC1 in the muscle cell regulates growth centrally, but not the autophagy process. Rüegg and his colleagues have now been able to refute this widespread thesis. In their current study, they examined the cellular processes in the muscles of mice in which mTORC1 was permanently switched on.

In aging mice in particular, the researchers observed progressive muscle disease that was due to worsened autophagy. Interestingly, by administering rapamycin, the researchers were able to reverse the symptoms of the disease. The muscle function of the mice normalized. Rapamycin is a substance that inhibits mTORC1 and thereby promotes cellular self-cleaning.

Accordingly, mTORC1 represents a superordinate authority that strictly coordinates the mechanism of autophagy and thus maintains the balance between muscle building and muscle breakdown. The scientists suspect that an overactive mTORC1 complex could also be responsible for the development of age-related muscle weakness in humans. A closer look at the mTORC1 regulatory system in the context of aging could therefore reveal new therapeutic ways of counteracting the breakdown of muscle structures.

MEDICA.de; Source: University of Basel