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Disrupting galectin-3 and NET-mediated microglia-neutrophil cross-talk suppresses pathological retinal angiogenesis
Ziyi Zhou1, Tianhao Yuan1, Jiaxing Sun1
1Department of Ophthalmology, Eye Institute of Chinese PLA, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.
Science Translational Medicine
|August 5, 2026
Summary
Neutrophil infiltration drives diabetic retinopathy progression by activating microglia and promoting pathological angiogenesis. Targeting this immune feedback loop with biomaterial-delivered therapies offers a novel therapeutic strategy for neovascular disorders.
Area of Science:
- Ophthalmology
- Immunology
- Biomaterials Science
Background:
- Pathological retinal neovascularization research traditionally focuses on growth factors and inflammation.
- Emerging evidence highlights the role of the retinal immune microenvironment in neovascular disorders.
- Understanding the immune-angiogenic interplay is crucial for developing new therapies.
Purpose of the Study:
- To investigate the role of the immune microenvironment in pathological retinal neovascularization.
- To identify specific immune cells and mediators involved in diabetic retinopathy progression.
- To explore novel therapeutic strategies targeting immune pathways for neovascular disorders.
Main Methods:
- Integrative analysis of single-cell RNA sequencing from human fibrovascular membranes.
- Analysis of multicohort clinical datasets.
- Mechanistic studies in mice with oxygen-induced retinopathy (OIR).
- Engineering of a photocurable hydrogel for sustained intravitreal drug delivery.
Main Results:
- Neutrophil infiltration was identified as an independent risk factor for diabetic retinopathy progression.
- Activated microglia secrete galectin-3 (GAL3), promoting neutrophil infiltration and pathological angiogenesis.
- A self-amplifying feedback loop between microglia and neutrophils sustains inflammation and drives neovascularization.
- Engineered hydrogel delivery of GAL3 and VEGF-neutralizing antibodies suppressed aberrant angiogenesis in OIR mice.
Conclusions:
- Retinal neovascularization is an immunovascular disorder.
- Microglia-neutrophil interactions mediated by GAL3 are critical drivers of pathological angiogenesis.
- Biomaterial-based strategies modulating the immune microenvironment show therapeutic potential for neovascular eye diseases.
