Blocking the protein PROX1 can help regenerate vision cells (such as photoreceptors in the retina) by lifting a developmental brake that normally prevents certain cells from becoming photoreceptors. Here's a breakdown of how this works:

What is PROX1?

PROX1 is a transcription factor — a protein that controls the expression of other genes. It plays a critical role in cell fate determination during development, including in the eye and retina.

In the retina:

PROX1 is expressed in horizontal cells and Müller glia (support cells).

It helps maintain cell identity, ensuring those cells don't transform into something else (like photoreceptors).

How does blocking PROX1 help regenerate vision cells?

Recent studies suggest that:

Müller glia, a type of retinal support cell, can potentially be reprogrammed into photoreceptors — the light-sensitive cells that are lost in diseases like retinitis pigmentosa or macular degeneration.

PROX1 suppresses this reprogramming. It keeps Müller glia in their support-cell role by inhibiting genes necessary for photoreceptor identity.

Blocking or deleting PROX1 lifts this suppression:

Müller glia can start expressing photoreceptor genes.

Some of them may begin to convert into rod or cone photoreceptors.

This leads to potential regeneration of vision in damaged or degenerative retinal conditions.

Research Example

A 2023 Nature study (by researchers at the University of Washington and UC Berkeley) showed that genetically deleting PROX1 in mouse models allowed Müller glia to activate a developmental program that turned them into functional photoreceptor-like cells.

This resulted in restored retinal responses to light.

It was one of the first demonstrations that endogenous glia can be reprogrammed into vision cells in mammals without introducing new genes — just by removing a single inhibitor (PROX1).

Caveats

These findings are still experimental and in animal models.

Full functional vision restoration in humans is not yet proven.