An old mouse hangs on a wire longer than usual, and after a run it doesn't collapse from exhaustion. The secret is that one tiny molecule called microRNA-128 was switched off in it. This molecule doesn't build proteins; it muffles the genes that muscles need. With age or in disease it muffles too much of what's useful, and muscles weaken. Block it, and muscles start working like they did in youth.
Scientists gave the mice a drug that sticks to microRNA-128 and keeps it from working. In old mice after this treatment, the time spent hanging on the wire rose by 66%, and running time by 58%. There was more muscle, less fat. In mice after a heart attack, the heart pumped more blood, and the scar shrank. In mice with inherited muscular dystrophy, muscle damage decreased. In every case, cells began burning energy better, and inflammation quieted down.
Why does this work? MicroRNA-128 is a master switch that, with age or in disease, starts muffling useful genes and turning on harmful ones. Remove that switch, and the cell returns to its youthful program. In people, genetic variants of this molecule are linked to grip strength and lung function, which means it matters for us too. It's still unknown which cells are responsible for the effect, and whether it extends life, but even today we can think about a drug against age-related muscle weakness, heart failure, and muscular dystrophy.
The miR-128-1 locus sits in a region of the genome that underwent one of the strongest selection events in Europeans: it is linked to lactose digestion, but also to obesity and diabetes. The very same genetic variation that helped ancestors survive famine may today speed up muscle aging.
Not published on arXiv. Here are its page, the PDF and the formalization: you can check it yourself, not only read our account.