Dual role of microglia and macrophages in the oxygen-induced retinopathy model: pathogenic mechanisms and therapeutic potential

Authors:Liu Wenhui, Gao Jingzhao, Su Lin, Li Xiaorong

Corresponding author: Li Xiaorong , Email: xiaorli@163.com

Published:2026-09-10

DOI:10.3760/cma.j.cn115989-20260331-00151

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ABSTRACT 

Oxygen-induced retinopathy (OIR) is an important animal model for retinal neovascular diseases. In recent years, increasing evidence has shown that alterations in the retinal immune microenvironment are involved throughout the development and progression of OIR, among which myeloid immune cells, such as microglia and macrophages, serve as key regulators linking inflammatory responses, vascular remodeling, and tissue repair. Myeloid cells in OIR exhibit marked heterogeneity in origin and functional plasticity: resident microglia participate in inflammatory responses through local proliferation and activation, whereas peripheral monocytes can be recruited into the retina under ischemic conditions and differentiate into macrophages. Current studies have shown that these cells are jointly regulated by glycolysis, lactate metabolism, succinate signaling, and inflammatory pathways, and may display predominantly pro-inflammatory or reparative functional states at different stages, thereby exerting a distinct dual role. On the one hand, they can amplify inflammatory responses, aggravate vascular obliteration, and promote pathological retinal neovascularization; on the other hand, they can contribute to vascular homeostasis, physiological revascularization, and tissue repair. Therefore, precise targeting of myeloid immune cells has gradually emerged as a new research focus. This review summarizes the origins, functional state transitions, metabolic-inflammatory regulatory networks, and dual roles of microglia and macrophages in OIR, and further outlines recent advances in related therapeutic strategies, with the aim of providing references for mechanistic studies and precision treatment of retinal neovascular diseases.

KEYWORDS：

Oxygen-induced retinopathy;Microglia;Macrophages;Retinal neovascularization;Immune microenvironment

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All articles published represent the opinions of the authors, and do not reflect the official policy of the Chinese Medical Association or the Editorial Board, unless this is clearly specified.

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Authors Info & Affiliations 

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Figures & Tables

Figure 1 Role and mechanism of macrophages and microglia in OIR A: Origin and phenotype of myeloid cells and retina-resident microglia (CX3CL1/CX3CR1 axis) and peripheral monocytes infiltrate and differentiate into macrophages through the CCL2/CCR2 axis, and both present M1 or M2 functional states. B: Metabolism-inflammation regulation Under hypoxia conditions, glycolysis is enhanced. Lactate drives the transformation of PFKFB3 to PRAGM phenotype and the YY1 lactoylation pathway. Succinic acid promotes pathological neovascularization through SUCNR1 signal. C: Cell interaction network Myeloid cells interact with Müller glial cells, vascular endothelial cells and photoreceptor cells to jointly regulate vascular occlusion and neovascularization

OIR: oxygen-induced retinopathy; CCL2: C-C motif chemokine ligand 2;CCR: C-C chemokine receptor;MIP: macrophage inflammatory protein;IL: interleukin;TNF-α: tumor necrosis factor alpha; Tlr2: Toll-like receptor 2; CX3CL1: chemokine (C-X3-C motif) ligand 1; CX3CR1: CX3C chemokine receptor 1;MMP: matrix metalloproteinase;NF-κB: nuclear factor κB;HIF-1α-Kit: hypoxia-inducible factor-1 α- KIT proto-oncogene;mTOR: mammalian rapamycin target protein; PFKFB3: 6-phosphate fructose-2-kinase/fructose-2,6-bisphosphatase3;PRAGM: pathological angiogenesis associated glycolytic macrophages/microglia; YY1: transcription factor Yinyang 1; SUCNR1: Succinate receptor 1

Figure 2 Therapeutic strategy targeting macrophages/microglia A: Phenotype regulation suppresses the M1 pro-inflammatory phenotype (NF-κB inhibitor PDTC and ferulic acid block the ROS/NF-κB axis), promote M2 repair phenotype, and accurately regulate M2 subgroups (Silencing lncRNA-MM2P, mannose-clodronic acid liposome MCL clears M2 phenotype and blocks IL-19) B: Metabolic reprogramming targets glycolysis (HK2 inhibitor icariin, PFKFB3/PKM2/MCTs/ACLY node), interfering with lactate signaling (DCA regulates lactate metabolism and blocks lactoylation at YY1K183 site), inhibits the SPP1-ITGA4 axis (Proliferation inhibitor abemaciclib) and succinine-SUCNR1-RBP4-VEGFR2 axis, supplemented with BH4 to block the TLR4-NF-κB/MAPK pathway C: Targeting and delivery Sirt2/Akt, RORγ/IL-17A blockade, furin protease, POSTN New targets such as (αvβ3/Akt) RNAi agent NK0144, S1P blocker sonepcizumab, TREM-1 peptide inhibitor, and long-acting GLP-1R agonist NLY01; Precision delivery systems include microglial exosomes (miR-27a-5p/Smad3), M2 exosomes, PS-modified STING inhibitor nanoparticles, peptide-gold nanohybrid P12, dendritic molecule D-TA and apoptotic T cell microvesicles LMPs D: multi-dimensional combination therapy ROCK inhibitors combined with MCP-1 blockade, phased intervention in early anti-inflammation and late repair promotion, endothelial cells-Müller cells-Tregs multicellular targeting

PDTC: pyrrolidine dithiocarbamate; ROS： Reactive oxygen species; NF-κB： Nuclear factor κB; MCL： Mannose-clodronate liposomes;IL: interleukin;STAT: signal transducer and activator of transcription;PPAR-γ: peroxisome proliferator-activated receptor γ;DDR2: discoid domain receptor 2;TGF-β: transforming growth factor beta;STING: interferon gene stimulating factor;lncRNA: long-chain non-coding RNA; MM2P: M2 macrophage polarization; HK2: hexokinase 2;AKT: protein kinase B;VEGF: vascular endothelial growth factor; PFKFB3: Fructose-6-phosphate-2-kinase/Fructose-2,6-bisphosphatase3; PKM2: Pyruvate kinase type M2;MCTs: monocarboxylic acid transporter;ACLY: ATP citrate lyase;ANAC: Acetyl-CoA and NAD+-related metabolic cycles;FGF: fibroblast growth factor;DCA: dichloroacetic acid; SPP1: secreted phosphoprotein 1; ITGA4: integrin alpha 4; SUCNR1: succinate receptor 1; RBP4: retinol binding protein 4; VEGFR2: vascular endothelial growth factor receptor 2; TLR4: Toll-like receptor 4; MAPK： Mitogen-activated protein kinase; BH4： Tetrahydrobiopterin; MCP-1： Monocyte chemoattractant protein-1;Tregs: regulatory T cells;Sirt2: silent information regulator 2;IGF-1: insulin-like growth factor 1; AGK2: specific inhibitor of Sirt2;RORγ: retinoic acid-related orphan receptor γ;POSTN: periostin; S1P: sphingosine-1-phosphate;TREM-1: myeloid cell trigger receptor 1;GLP-1R: glucagon-like peptide-1 receptor;PS: phosphatidylserine;LMPs: lymphocyte-derived microvesicles

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