ArticleNature communications2026
Therapeutic modulation of the vitreoretinal fibrosis microenvironment in female mice using engineered macrophage-derived extracellular vesicles.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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15 authors.
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Abstract
Vitreoretinal fibrosis, a hallmark of proliferative vitreoretinopathy (PVR) triggered by retinal detachment or ocular trauma, necessitates surgery. Through data mining of the vitreoretinal fibrosis microenvironment in PVR patients and mice, showing elevated transforming growth factor β1 (TGFβ1) and M2 macrophage enrichment, we designed and engineered extracellular vesicles that conferred anti-fibrotic efficacy against PVR. These M1 macrophage-derived vesicles (M1evs) were conjugated with anti-TGFβ1 antibodies (aT) via MMP-cleavable linkers (aT-cl-M1ev, termed ACE). Upon intravitreal injection in female PVR model mice, ACE selectively accumulates in lesions, where released antibodies neutralize TGFβ1 and M1evs inhibit M2 macrophage polarization, modulating the microenvironment to diminish vitreoretinal fibrosis. Further incorporating anti-platelet-derived growth factor receptor antibodies yields aTP-cl-M1ev (ACE
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