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For years, researchers have found that young animals tend to recover better from tissue damage than adults. Despite witnessing this phenomenon, scientists were unsure of why it occurred. Now, in a new study, a research team discovered that a gene called Lin28a appears to be responsible for repairing tissue damage. The problem is, Lin28a is only active in embryos and not in adults. The researchers believe that this gene could help them find ways of improving the time it takes adults to recover from tissue damage.

"It sounds like science fiction, but Lin28a could be part of a healing cocktail that gives adults the superior tissue repair seen in juvenile animals," the senior author of the study, George Daley of Boston Children's Hospital and Harvard Medical School, said.

For this study, Daley and his team of researchers analyzed the role of Lin28a. They explained that since Lin28a helps regulate growth and development in the youth, it could be responsible for faster tissue repair time. As animals age, their levels of the Lin28a protein start to decline. In order to study Lin28a, the research team reactivated the gene in adult mice. They observed that the activation of the gene promoted hair regrowth in mice that the researchers had shaved. The gene also helped promote tissue repair in the mice's injured ears and digits. Furthermore, the Lin28a protein appeared to stimulate cell proliferation and migration, which are both necessary for tissue repair.

"We were surprised that what was previously believed to be a mundane cellular 'housekeeping' function would be so important for tissue repair," said study author Shyh-Chang Ng of Harvard Medical School. "One of our experiments showed that bypassing Lin28a and directly activating mitochondrial metabolism with a small-molecule compound also had the effect of enhancing wound healing, suggesting that it could be possible to use drugs to promote tissue repair in humans."

The study, "Lin28a enhances tissue repair by reprogramming cellular metabolism," was published in Cell by Cell Press.