MicroRNA Target Shows Promise for Restoring Muscle in Old Mice

Using antisense oligonucleotides to block miR-128-3p restored muscle mass and function in aged mice, according to the study. The same intervention improved heart function and limited adverse remodeling after myocardial infarction, and it reduced skeletal and cardiac muscle pathology in mouse and pig models of Duchenne muscular dystrophy. The treatment activated mitochondrial programs and suppressed inflammatory and fibrotic signaling, a pattern resembling known longevity interventions.

Interest in preserving muscle has grown partly because GLP-1 receptor agonists can cause calorie restriction and muscle loss. That attention may also aid research into age-related frailty. The miR-128-1 locus lies in a human haplotype tied to grip strength, lung function, and cardiometabolic traits.

Blocking miR-128-3p with antisense oligonucleotides boosted muscle size and performance in old mice. In other models, it improved heart function after myocardial infarction, limited harmful remodeling, and eased skeletal and cardiac muscle pathology in mouse and pig Duchenne muscular dystrophy. It switched on mitochondrial programs and quieted inflammatory and fibrotic signals, echoing longevity interventions. Elenae Therapeutics is first targeting severe, less common conditions.