Preventing muscle atrophy

Dr. Stephen Burden and colleagues demonstrate that the DNA-binding protein, Runx1 (AML1), directs the expression of 29 genes involved in the prevention of skeletal muscle wasting. Using mice deficient in runx1 specifically in skeletal muscle cells, the researchers determined that Runx1 activation is necessary to sustain muscle by limiting the autophagy of denervated myofibers.

Dr. Burden believes that their findings “raise the intriguing possibility that congenital myopathies, which do not follow simple Mendelian inheritance or become evident only late in life, may require two initiating events: a decrease in muscle activity, due to trauma, aging, or immobilization, as well as a mutation in Runx1 or its target genes.”