Promoting muscle regeneration in a mouse model of muscular dystrophy

Duchenne muscular dystrophy (DMD) is a degenerative skeletal muscle disease caused by mutations in the protein dystrophin. Dystrophin functions to protect muscle cells from injury and loss of functional dystrophin results in break down and loss of muscle cells. A cellular signal relay system, known as a MAP kinase cascade, regulates the function of muscle stem cells, serving as a source of the new cells that are required for muscle regeneration.

In this issue of the Journal of Clinical Investigation, researchers led by Anton Bennett at Yale University identified the protein MKP-5 as a negative regulator of MAP kinase cascades in muscle stem cells. Loss of MKP-5 in a mouse model of DMD enhanced the development of new muscle cells (myogenesis) and helped prevent muscle degeneration.

These results identify MKP-5 as an important suppressor of myogenesis and suggest that therapeutics that inhibit MKP-5 could be useful in the treatment of degenerative muscle diseases.

More information: Improved regenerative myogenesis and muscular dystrophy in mice lacking MKP-5, J Clin Invest. doi:10.1172/JCI64375

Related Stories

Recommended for you

'Google Maps' for the body: A biomedical revolution

date 14 hours ago

A world-first UNSW collaboration that uses previously top-secret technology to zoom through the human body down to the level of a single cell could be a game-changer for medicine, an international research ...

New compounds could offer therapy for multitude of diseases

date 15 hours ago

An international team of more than 18 research groups has demonstrated that the compounds they developed can safely prevent harmful protein aggregation in preliminary tests using animals. The findings raise hope that a new ...

User comments

Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Click here to reset your password.
Sign in to get notified via email when new comments are made.