A team at The University of Texas Southwestern Medical Center at Dallas has shown that deletion of class IIa histone deacetylases prevents muscle atrophy after nerve damage.1 The result suggests that inhibitors of these molecules could help treat neuromuscular diseases, a hypothesis the researchers are testing by deleting class IIa HDACs in a mouse model of amyotrophic lateral sclerosis.
ALS and other neuromuscular diseases damage motor neurons, causing denervation that leads to muscle atrophy. Previous studies by UT Southwestern's Eric Olson, professor and chairman of molecular biology, identified a compensatory regeneration pathway that acts to recover the neuromuscular junction after nerve injury.2 However the signaling pathway leading to muscle atrophy remained poorly understood.
Now, Olson's lab has identified the specific factors involved in denervation-mediated muscle atrophy. The team's first clue came from previous experiments demonstrating that