ArticleNature communications2026
ROS-autocatalytic nanoplatform interfering astrocyte-cancer crosstalk and enhancing glioblastoma therapy.
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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9 authors.
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Abstract
Glioblastoma (GBM) remains incurable and exhibits exceptionally high metabolic demands, driving the evolution of hyperactive mitochondrial systems within tumors. In parallel, mitochondrial transfer from astrocytes to cancer cells fuels metabolic reprogramming and enhances GBM tumorigenicity. These malignant traits markedly constrain therapeutic efficacy and patient survival. Herein, we report a dehydroascorbic acid (DHA)-functionalized, ROS-responsive, ferrocene-integrated polymer nanoplatform (GS@DFP) co-loaded with S-Gboxin and Galunisertib, simultaneously targeting GBM mitochondria and mitochondrial transfer in astrocyte-cancer cell crosstalk. After crossing the blood-brain barrier (BBB) through Glut1-mediated transport enabled by DHA, GS@DFP responds to elevated intracellular reactive oxygen species (ROS) levels in GBM to trigger payload release and initiate Fenton reactions. S-Gboxin inhibits mitochondrial complex V and depletes ATP, whereas Galunisertib downregulates TGF-β/SMAD-driven thrombospondin-1 (TSP-1) expression, suppressing tumor microtube (MT) formation and thereby reducing astrocyte-to-GBM mitochondrial transfer. Notably, TGF-β inhibition also reprograms the immunosuppressive tumor microenvironment (TME). This work establishes a multifunctional nanoplatform that targets mitochondrial vulnerabilities and intercellular crosstalk, offering a translatable strategy for enhancing GBM therapy.
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