ArticleJournal of pharmaceutical analysis2024
Platelet membrane biomimetic nanomedicine induces dual glutathione consumption for enhancing cancer radioimmunotherapy.
Article in Journal of pharmaceutical analysis, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Herb-derived immunometabolic modulators: traditional Chinese medicine at the crossroads of metabolism and antitumor immunity.Chinese medicine · 2026Review
- Glycolysis in the tumor microenvironment shapes dendritic cell function and antitumor immunity.Frontiers in immunology · 2026Review
- Engineering design of platelet-mimicking therapeutic systems: multilevel biomimicry, gating strategies, and translational boundaries.Frontiers in bioengineering and biotechnology · 2026Review
- Tumor-microenvironment triggered Mn-Gd based nanosystem for breast carcinoma suppression via synergistic radiotherapy and glutathione-depleting along with glucose oxidase combination enhanced Ros storm.Journal of nanobiotechnology · 2025Article
- Recent advances in biomimetic nanodelivery systems for cancer Immunotherapy.Materials today. Bio · 2025Review
- From Blood to Therapy: The Revolutionary Application of Platelets in Cancer-Targeted Drug Delivery.Journal of functional biomaterials · 2025Review
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Authors and funding
8 authors.
Funding
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Abstract
Radiotherapy (RT) is one of the most common treatments for cancer. However, intracellular glutathione (GSH) plays a key role in protecting cancer from radiation damage. Herein, we have developed a platelet membrane biomimetic nanomedicine (PMD) that induces double GSH consumption to enhance tumor radioimmunotherapy. This biomimetic nanomedicine consists of an external platelet membrane and internal organic mesoporous silica nanoparticles (MON) loaded with 2-deoxy-D-glucose (2-DG). Thanks to the tumor-targeting ability of the platelet membranes, PMD can target and aggregate to the tumor site, which is internalized by tumor cells. Within tumor cells overexpressing GSH, MON reacts with GSH to degrade and release 2-DG. This step initially depletes the intracellular GSH content. The subsequent release of 2-DG inhibits glycolysis and adenosine triphosphate (ATP) production, ultimately leading to secondary GSH consumption. This nanodrug combines dual GSH depletion, starvation therapy, and RT to promote immunogenic cell death and stimulate the systemic immune response. In the bilateral tumor model in vivo, distal tumor growth was also well suppressed. The proportion of mature dendritic cells (DC) and CD8
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