ArticleJournal of nanobiotechnology2025
Microglia-specific interleukin-4 delivery by engineered extracellular vesicles restores inner blood-retinal barrier in diabetic retinopathy via GAS6-MERTK pathway.
Article in Journal of nanobiotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Small Extracellular Vesicles from Neural Cells: Physiological and Pathological Roles, and Potential in Neurodegenerative Therapy.Advanced healthcare materials · 2026Review
- The gut-retina axis in diabetic retinopathy: a new paradigm for pathogenesis and therapeutic intervention.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Maintaining a balanced polarization of microglia is one of the most potential therapeutic approaches for diabetic retinopathy (DR). However, reliable, sustained, effective, and controllable microglial regulation still faces formidable challenges. Here, inspired by the bioavailability and modifiability of extracellular vesicles (EV), we developed an interleukin 4 (IL4)-encapsulated and M1 microglia-targeting EV platform (IL4@CHHSSSARC-EV) for rescuing inner blood-retina barrier (iBRB) deterioration in DR. Delivery of IL4 via IL4@CHHSSSARC-EV enhanced not only the stability of IL4, but also the efficacy of anti-inflammatory phenotype (M2) shift in vitro and in vivo due to their selectivity to pro-inflammatory (M1) microglia. Treatment with IL4@CHHSSSARC-EV significantly ameliorated pathological angiogenesis and iBRB breakdown caused by hypoxia and ischemia in oxygen-induced retinopathy models, and potently minimized leakage, bleeding, lesions, pericyte loss and leukocyte adherence of vascular network in streptozotocin-induced diabetic mice with a high safety profile. Mechanistically, IL4@CHHSSSARC-EV facilitated microglial phagocytic capacity through GAS6-MERTK signaling, thereby engulfing aberrant vessels and disrupting the reciprocal crosstalk between microglia and pathological vasculature. Our study demonstrated that engineering EV as an enduring, efficient and safe implement for manipulating microglia provided a potential strategy for a rebalanced immune profile in DR.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.