A new study found that a novel mRNA-based therapy that targets a protein called RUNX1 may be able to prevent blindness and scarring from proliferative vitreoretinopathy (PVR), a disease caused by a traumatic eye injury or surgery like a retinal detachment repair that currently lacks effective treatments other than additional surgical procedures.
A new study found that a novel mRNA-based therapy that targets a protein called RUNX1 may be able to prevent blindness and scarring from proliferative vitreoretinopathy , a disease caused by a traumatic eye injury or surgery like a retinal detachment repair that currently lacks effective treatments other than additional surgical procedures.
PVR is scar tissue that forms inside the eye, commonly after eye trauma, that can contract and detach the retina. This pathologic scar tissue response, rather than the eye injury itself, is what can lead to blindness. The researchers developed and studied the efficacy of various mRNAs encoding for proteins related to the scar tissue formation to see which might be useful as a therapeutic. To develop a treatment for PVR, the researchers targeted a protein called RUNX1 that regulates the expression of a gene that turns eye cells into scar tissue.
The researchers consider this study a proof of concept that suggests that the mRNA approach may be useful for PVR and other eye diseases. The study's limitations include that the experiments were in cellular and preclinical models. This approach has not been tested in human subjects. The technology itself may have some limitations as mRNA doesn't remain in the cell very long making proteins.
Study co-first author William P. Miller, PhD, a postdoctoral fellow in the Department of Ophthalmology at Mass Eye and Ear and Harvard Medical School, noted,"This work is the result of substantial effort put forth by our team, encompassing multiple experts across several different fields. It demonstrates novel applications of mRNA technology in ophthalmology and has implications for other aspects of medicine as well."Michael O’Hare, William P.
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