Related Experiment Video
Updated: Oct 17, 2025

An Ex Vivo Tissue Culture Model for Fibrovascular Complications in Proliferative Diabetic Retinopathy
Published on: January 25, 2019
Cellular targets in diabetic retinopathy therapy
María Lucía Rodríguez1, Iván Millán2, Ángel Luis Ortega3
1Department of Physiology, Faculty of Pharmacy, University of Valencia, Burjassot 46100, Valencia, Spain.
Abstract:
Despite the existence of treatment for diabetes, inadequate metabolic control triggers the appearance of chronic complications such as diabetic retinopathy. Diabetic retinopathy is considered a multifactorial disease of complex etiology in which oxidative stress and low chronic inflammation play essential roles. Chronic exposure to hyperglycemia triggers a loss of redox balance that is critical for the appearance of neuronal and vascular damage during the development and progression of the disease. Current therapies for the treatment of diabetic retinopathy are used in advanced stages of the disease and are unable to reverse the retinal damage induced by hyperglycemia. The lack of effective therapies without side effects means there is an urgent need to identify an early action capable of preventing the development of the disease and its pathophysiological consequences in order to avoid loss of vision associated with diabetic retinopathy. Therefore, in this review we propose different therapeutic targets related to the modulation of the redox and inflammatory status that, potentially, can prevent the development and progression of the disease.
Insights
Diabetic retinopathy, a complication of diabetes, involves oxidative stress and inflammation. Targeting redox and inflammatory pathways may prevent vision loss by addressing early disease development.
Area of Science:
- Ophthalmology
- Endocrinology
- Molecular Medicine
Background:
- Diabetic retinopathy (DR) is a major complication of diabetes mellitus, often leading to vision loss.
- Inadequate glycemic control exacerbates DR, driven by oxidative stress and chronic inflammation.
- Hyperglycemia-induced redox imbalance damages retinal neurons and vasculature.
Purpose of the Study:
- To review current understanding of diabetic retinopathy pathogenesis.
- To highlight the limitations of existing treatments for diabetic retinopathy.
- To propose novel therapeutic targets for early intervention in diabetic retinopathy.
Main Methods:
- Literature review focusing on the roles of oxidative stress and inflammation in diabetic retinopathy.
- Analysis of current therapeutic strategies and their efficacy in advanced disease stages.
- Identification of potential molecular targets for preventative therapies.
Main Results:
- Oxidative stress and chronic inflammation are key drivers of diabetic retinopathy.
- Current therapies are often insufficient, acting only in advanced stages and unable to reverse damage.
- Early intervention strategies targeting redox and inflammatory pathways show promise.
Conclusions:
- Modulating redox and inflammatory status presents a promising avenue for preventing diabetic retinopathy.
- Targeting these pathways may halt disease progression and prevent vision loss.
- Further research into early-stage therapeutic interventions is urgently needed.
Related Concept Videos
Diabetes: Management and Pharmacotherapy
Insulin remains the cornerstone of treatment for most patients with type 1 and many...
Targets for Drug Action: Overview
Receptors are either membrane-spanning or intracellular proteins, which upon binding a ligand, get activated and transmit the signal downstream to elicit a response. Drugs bind receptors, either mimicking the action of endogenous ligands or blocking the receptor activity to bring about a modified response. Nearly 35% of approved drugs target the G...
Pathophysiology of Diabetes
Type 1 diabetes is characterized by autoimmune-mediated destruction of pancreatic β cells, with environmental factors potentially triggering this process in genetically susceptible individuals. Despite many not having a family history, certain genes increase susceptibility,...

