# Classical and Innovative Evidence for Therapeutic Strategies in Retinal Dysfunctions

## TL;DR

This paper reviews traditional and new therapeutic strategies for retinal diseases, focusing on inflammation, oxidative stress, and emerging approaches like cell secretomes and gut-retina interactions.

## Contribution

The paper introduces novel therapeutic approaches such as mesenchymal cell secretomes, noncoding RNAs, and the gut-eye axis for retinopathy treatment.

## Key findings

- Mesenchymal cell secretomes may reduce oxidative stress and cell death in retinal cells.
- Noncoding RNAs show potential as therapeutic targets and biomarkers for retinopathies.
- Gut microbiota alterations are linked to ocular diseases, suggesting a gut-eye axis.

## Abstract

The human retina is a complex anatomical structure that has no regenerative capacity. The pathogenesis of most retinopathies can be attributed to inflammation, with the activation of the inflammasome protein platform, and to the impact of oxidative stress on the regulation of apoptosis and autophagy/mitophagy in retinal cells. In recent years, new therapeutic approaches to treat retinopathies have been investigated. Experimental data suggest that the secretome of mesenchymal cells could reduce oxidative stress, autophagy, and the apoptosis of retinal cells, and in turn, the secretome of the latter could induce changes in mesenchymal cells. Other studies have evidenced that noncoding (nc)RNAs might be new targets for retinopathy treatment and novel disease biomarkers since a correlation has been found between ncRNA levels and retinopathies. A new field to explore is the interaction observed between the ocular and intestinal microbiota; indeed, recent findings have shown that the alteration of gut microbiota seems to be linked to ocular diseases, suggesting a gut–eye axis. To explore new therapeutical strategies for retinopathies, it is important to use proper models that can mimic the complexity of the retina. In this context, retinal organoids represent a good model for the study of the pathophysiology of the retina.