Ferroptosis in diabetic retinopathy: from pathogenic mechanisms to translational prospects

TL;DR

This review explores how a type of cell death called ferroptosis contributes to diabetic retinopathy and suggests possible new treatments.

Contribution

The paper provides a comprehensive overview of ferroptosis mechanisms and its role in diabetic retinopathy, highlighting potential therapeutic strategies.

Findings

Ferroptosis is increasingly recognized as a key player in the progression of diabetic retinopathy.

Abnormal iron metabolism and related signaling pathways are linked to ferroptosis in DR.

Potential ferroptosis inhibitors may offer new treatment options for diabetic retinopathy.

Abstract

Diabetic retinopathy (DR) is a common microvascular complication of diabetes. Despite ongoing revisions in the prevention and treatment of DR, optimal treatment strategies have yet to be established. Revealing the pathological changes and molecular mechanisms of DR is the cornerstone for exploring new therapeutic strategies. Ferroptosis, a new type of programmed cell death proposed in recent years, is characterized mainly by reactive oxygen species and iron-mediated lipid peroxidation. As studies progress, growing evidence has highlighted the involvement of ferroptosis, a newly identified programmed cell death pathway, in the development and pathological mechanisms of DR. The purpose of this review is to discuss the known underlying mechanisms of ferroptosis and elucidate its role in the pathogenesis of DR. Additionally, it explores the abnormal manifestations of iron metabolism and related signaling pathways in DR. Finally, we also summarize the potential compounds that may act as ferroptosis inhibitors in DR in the future. By synthesizing these aspects, this review aims to provide insights for a deeper understanding of the relationship between ferroptosis and DR, as well as potential prevention and treatment strategies.

Figures