Blindness: Reactivating Inactive Genes Can Regenerate Damaged Retinas

In mammals, the retina is one of the few tissues where damage is irreparable. However, a spontaneous regeneration mechanism in mammals could be activated artificially so that patients could eventually regain their sight.



The human body – and more generally the body of mammals – is an admirable machine, that is complex and resilient because of its ability to heal and self-repair. Fortunately, we can safely venture outside our homes without fear of the slightest scratch leaving its mark forever. However, not all tissues are created equally in the healing process.

Read Also: An Artificial Retina to Restore Sight Could Soon Become a Reality

Although most tissues have the opportunity to regenerate with due care, this is not true for the retina. Blindness, age-related macular degeneration, retinitis pigmentosa are all diseases that can be delayed rather than cured or prevented by treatment.

However, many cold-blooded vertebrates do not have the same problem. Studies on zebrafish, with which we share about 70% of our genome, show that zebrafish is able to regenerate damage to its retina by a specific set of genes.

A lost function

The good news is that a recent discovery suggests that mammals also have a (dormant) version of the materials needed for this type of healing. “Regeneration seems to be the standard method of repair, but the loss of this ability has occurred at various points in the evolutionary tree,” says Seth Blackshaw, the corresponding author of the study, who appeared in Science magazine.

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Our retina contains Müller’s glia, support cells that ensure the structural and functional integrity of cones and stems. They perform many functions, including replacing damaged receptors in some fish and reptiles.

A deactivated function

When it is necessary to produce new cells, the body temporarily stops producing nuclear factor I (NFI), a protein that denies the cell access to certain DNA sequences, so that glial cells can transform and divide into completely new receptors.

This process can even occur in mammals but is usually short-lived due to the rapid reactivation of NFI, which interrupts the work of glia. Researchers have thus tried to prolong the duration of the inactivity of this nuclear factor in rats, with amazing results.

Read Also: Regular Check-Ups Are Necessary to Prevent the Worsening of Glaucoma.

“In general, our results suggest that the regenerative potential is present in mammals, including humans, but has so far been deactivated by some evolutionary pressure,” says Blackshaw. These results represent only a small fraction of the immense distance that has to be traveled to repair the human retina but represent an encouraging new breakthrough in biology and medicine.


Gene regulatory networks controlling vertebrate retinal regeneration

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