Related Experiment Video
Updated: Mar 2, 2026
Author Spotlight: Understanding Retinal Vessel Resilience and Disease Progression
Published on: January 12, 2024
Protective treatments and their target retinal ganglion cells in diabetic retinopathy
Jing Zhang1, Rong Liu1, Hong-Yu Kuang1
1Department of Endocrinology, The First Clinical Hospital of Harbin Medical University, Harbin, 150001, China.
Abstract:
Diabetic retinopathy(DR)is one of the complications of diabetes which could cause severe vision loss. Retinal ganglion cell(RGC)injury has been confirmed prior to micro-vascular damage. Over the past few decades, a number of animal and clinical studies have confirmed that RGC impairment leads to an early deterioration of vision in DR. Inhibition of aldose reductase (AR), advanced glycation end product (AGE), oxidative stress, glutamate toxicity, and an inflammatory response may play important roles in protecting RGCs in DR. Furthermore, nicotinamide mononucleotide adenylyl transferase-1 (Nmnat1), neurotrophins and neurotrophic factors may become new therapeutic targets. Photobiomodulation (PBM) may be used as adjunctive therapy in protective treatment of RGCs. In this review, we highlight and discuss protective treatments and their targets which have shown great promise for treatment of RGC injury in DR.
Insights
Diabetic retinopathy (DR) causes vision loss through retinal ganglion cell (RGC) injury. This review explores promising protective treatments targeting RGCs, including inhibiting inflammation and oxidative stress.
Area of Science:
- Ophthalmology
- Neuroscience
- Endocrinology
Background:
- Diabetic retinopathy (DR) is a major complication of diabetes, leading to severe vision loss.
- Retinal ganglion cell (RGC) injury precedes microvascular damage in DR, causing early vision deterioration.
- Understanding RGC injury mechanisms is crucial for developing effective DR treatments.
Purpose of the Study:
- To review and discuss protective treatments and their molecular targets for RGC injury in diabetic retinopathy.
- To highlight emerging therapeutic strategies for preserving vision in DR patients.
Main Methods:
- Comprehensive literature review of animal and clinical studies on RGC protection in DR.
- Analysis of potential therapeutic targets including aldose reductase (AR), advanced glycation end products (AGEs), oxidative stress, and inflammation.
- Evaluation of novel targets like nicotinamide mononucleotide adenylyl transferase-1 (Nmnat1) and neurotrophic factors.
Main Results:
- Inhibition of AR, AGEs, oxidative stress, glutamate toxicity, and inflammation are key protective strategies for RGCs in DR.
- Nmnat1, neurotrophins, and neurotrophic factors represent promising new therapeutic targets.
- Photobiomodulation (PBM) shows potential as an adjunctive therapy for RGC protection.
Conclusions:
- Multiple pathways are involved in RGC injury in DR, offering diverse targets for intervention.
- Targeting these pathways and exploring novel agents like Nmnat1 and PBM can significantly improve RGC protection.
- This review consolidates promising strategies for the future treatment of RGC injury in diabetic retinopathy.
