ArticleMaterials today. Bio2026
Brain-targeting nanoplatform repurposing silymarin for enhanced GBM immunotherapy via synergistic mitochondrial suppression.
Article in Materials today. Bio, 2026. 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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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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Who cites it
2 citing papers in PubMed.
- Lactoferrin and Nanotechnology: New Insights Into Glioblastoma Therapy.CNS neuroscience & therapeutics · 2026Review
- Dietary polyphenols and nutritional modulators in glioblastoma: mechanistic promise and translational barriers.Frontiers in nutrition · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBM), a highly malignant central nervous system tumor, poses a major therapeutic challenge due to the poor blood-brain barrier (BBB) permeability and an immunosuppressive tumor microenvironment. Notably, silymarin, a natural compound known for its anti-inflammatory and liver-protective properties, has emerged as a promising candidate for GBM immunotherapy through the inhibition of glycolysis and induction of mitochondrial damage. In this study, we developed a silymarin-repurposed, site-specific delivery photo-chemotherapy nanoplatform, designed to synergistically suppress mitochondria for efficient GBM immunotherapy. The platform utilizes a self-assembly strategy incorporating brain-targeted lactoferrin (LF), triphenylphosphine-modified chlorin e6 (TCe6), and silymarin. Mechanistically, LF facilitates targeted binding to low-density lipoprotein receptor-related protein-1 (LRP1), enabling BBB penetration and inducing mitochondrial dysfunction in GBM cells through TCe6-mediated intracellular reactive oxygen species (ROS) generation and silymarin-induced glycolysis suppression. This mitochondrial dysfunction triggers the activation of the AMPK pathway, leading to the degradation of programmed cell death ligand-1 (PD-L1) and the activation of the cGAS-STING pathway, thereby enhancing the anti-tumor immune response. As anticipated, this nanoplatform significantly improves BBB permeability and antitumour immunity, providing an innovative drug repurposing strategy for effective GBM immunotherapy.
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Registered trials
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