ArticleACS nano2026
A Redox-Responsive Selenium-Containing Nanomedicine Enables Dual Antioxidant System Inhibition to Overcome Platinum Resistance and Enhance Immunotherapy in Bladder Cancer.
Article in ACS nano, 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.
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.
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Who cites it
2 citing papers in PubMed.
- Cell Membrane-Engineered FePDA Nanoparticles Integrate Ferroptosis and Antitumor Immunity.Small (Weinheim an der Bergstrasse, Germany) · 2026Article
- Targeted Nanoparticles for PROTAC-Mediated JAK1/JAK2 Degradation for Bladder Cancer Treatment.International journal of nanomedicine · 2026Article
Corrections and comments
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Authors and funding
18 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cisplatin-based chemotherapy is the standard first-line treatment for bladder cancer, but its efficacy is limited by drug resistance. Immune checkpoint blockades have emerged as promising therapeutic options; however, their benefits are restricted by the immunosuppressive tumor microenvironment and low response rates. Overcoming both platinum resistance and immune evasion remains a major therapeutic challenge. In this study, we developed NP2, a redox-responsive amphiphilic selenium-containing polymer that encapsulates a platinum(IV) prodrug. NP2 disassembles in response to intracellular glutathione (GSH), releasing active cisplatin to induce DNA damage and apoptosis. Concurrently, diselenide bonds deplete GSH, disturbing the GSH antioxidant system, while selenium residues suppress thioredoxin (Trx) reductase, blocking the Trx system. This dual inhibition prevents cisplatin inactivation, enhances chemotherapy efficacy, and elevates the level of reactive oxygen species (ROS). Therefore, the increased ROS induces immunogenic cell death, promotes dendritic cell maturation, and activates adaptive immunity, thereby converting "immune-cold" tumors into "immune-hot" tumors. Further, NP2 suppressed tumor growth, remodeled the immune microenvironment, and upregulated programmed death-ligand 1 (PD-L1) expression
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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 OpenQuestion graph.