From the article: For some creatures, a lost body part is not necessarily a permanent affair. Salamanders can regrow limbs and zebrafish can rebuild their retinas. Yet mammals — including humans — are largely stuck with what they’re born with. When vision is lost to degenerative diseases like retinitis pigmentosa, it stays lost.
But a team of scientists in South Korea may have found a way to change that.
In a discovery that could reshape how we treat blindness, the researchers at the Korea Advanced Institute of Science & Technology (KAIST) have developed a therapy that restores vision by prompting the retina to heal itself. The treatment, tested in mice, triggered long-term regeneration of nerve cells in the retina — something previously thought impossible in mammals.
Inside our eyes, a special kind of cell called Müller glia keeps watch. These cells protect the retina, maintaining its structure and supporting its neurons. In fish and amphibians, they do even more. They can transform into new neurons, repairing retinal damage. In mammals, however, that regenerative process is switched off. Once the retina is harmed, it stays that way.
Why can’t our Müller glia do the same? The answer, it turns out, may lie in an unexpected molecular stowaway.
The new study, published in Nature Communications, zooms in on a protein called Prox1. In mammals, this protein appears to travel between cells and land inside Müller glia, where it acts like a molecular handbrake, preventing these cells from reprogramming into neuron-generating machines.