ArticleJournal of extracellular vesicles2025
M2 Macrophage-Derived Migrasomes Mediate Ischaemia-Induced Retinal Neovascularization by Targeting TREM2.
Article in Journal of extracellular vesicles, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The trial behind it
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Who cites it
3 citing papers in PubMed.
- Microglial TSPAN4-Dependent Migrasomes Promote Pathological Retinal Neovascularization via Immune-Vascular Crosstalk.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- TREM2: A Potential Target for the Targeted Therapy of Metabolic Diseases.Mediators of inflammation · 2026Review
- M2 Macrophage-Derived Migrasomes Mediate Ischaemia-Induced Retinal Neovascularization by Targeting TREM2.Journal of extracellular vesicles · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Retinal neovascular diseases are leading causes of global blindness. Migrasomes, organelles released during cell migration, play a role in intercellular communication and are present in M2 macrophages, which are critical to the pathology of retinal neovascular diseases. This study investigates the involvement of M2 macrophage-derived migrasomes in ischaemia-induced retinal neovascularization (RNV). Migrasomes are isolated from macrophages and characterized by Western blotting and transmission electron microscopy. Compared with controls, M2 macrophage-derived migrasomes significantly enhance human retinal microvascular endothelial cell (HREC) functions by Cell Counting Kit-8, transwell, and tube formation assays, and markedly contribute to the pathological retinal angiogenesis of oxygen-induced retinopathy (OIR) mice. Triggering receptor expressed on myeloid cells 2 (TREM2) is selected as the potential downstream target of M2 macrophage-derived migrasomes by proteomic analysis. Moreover, the depletion of M2 macrophages in OIR retinas reduces the levels of migrasomes and TREM2. BTC and PLA1A overexpression in HRECs could attenuate decreased HREC functions induced by sh-TREM2 M2 macrophage-derived migrasomes. These findings demonstrate that TREM2-enriched M2 macrophage-derived migrasomes contribute to pathological RNV in vivo and positively regulate HREC functions in vitro through targeting TREM2-BTC/PLA1A, which may serve as biomarkers and therapeutic targets for retinal neovascular diseases.
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Registered trials
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