ArticleJournal of extracellular vesicles2026
Targeted Delivery of GLUT1 Inhibitor via Macrophage Nanovesicles for Pulmonary Arterial Hypertension Therapy.
Article in Journal of extracellular vesicles, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Deficiency of GLUT1 in macrophages reprograms tumor-associated macrophages to normalize tumor vasculature and retards the progression of tumors.International journal of biological sciences · 2026Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Pulmonary arterial hypertension (PAH) is a lethal disease characterized by inflammation-driven vascular remodelling, with a lack of precise intervention strategies targeting pro-inflammatory M1 macrophages' glycolytic metabolic reprogramming. This study introduced Mac@WZB117, a macrophage membrane-camouflaged nanovesicle delivering the GLUT1 inhibitor WZB117, specifically targeting M1 macrophages for PAH treatment. In mouse models of PAH induced by MCT and SU5416 combined with hypoxia, Mac@WZB117 effectively targeted pulmonary vascular lesions, leading to a significant reversal of arterial thickening and collagen deposition. Molecular analyses indicated a downregulation of GLUT1 expression in M1 macrophages, along with a polarization shift from M1 to M2. Furthermore, intervention with Mac@WZB117 reshaped the immuno-metabolic lineage by inhibiting glycolysis, lipid metabolism and TGF-β signalling pathways. Spatial transcriptomics analysis confirmed the spatial reorganization of hyperactive M1 macrophages from lesion regions. Overall, Mac@WZB117 delivers WZB117 precisely to M1 macrophages, suppressing their pro-inflammatory and metabolic functions to remodel the immune microenvironment and reverse vascular structural changes, suggesting a promising therapeutic approach for PAH and other immuno-metabolic diseases.
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What Socratic holds
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.