ArticleInternational journal of nanomedicine2025
Pleiotropic Multi-Drug Co-Assembled Nanocomposites Offer Protection Against Doxorubicin-Induced Cardiotoxicity.
Article in International journal of nanomedicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. 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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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
2 citing papers in PubMed.
- Mitochondrial dysfunction-driven PANoptosis in doxorubicin-induced cardiotoxicity: mechanistic insights and intervention strategies.Frontiers in pharmacology · 2026Review
- Self-Assembled Nanoparticles: Overcoming Limitations of Conventional Nanomedicines for Enhanced Tumor Therapy.International journal of nanomedicine · 2025Review
Corrections and comments
- Erratum issued
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Doxorubicin (DOX) is a first-line chemotherapeutic agent, yet its clinical utility is limited by doxorubicin-induced cardiotoxicity (DIC), a dose-dependent side effect. Current drug delivery strategies fail to prevent off-target accumulation of DOX in cardiac tissue, necessitating innovative therapeutic approaches that protect the heart without compromising antitumor efficacy through targeted cardioprotection. Methods: We developed a multifunctional self-assembled nanoplatform (PGPP/NPs) via co-assembly of ginsenoside Rb1, probucol (PB), and a phosphoinositide 3-kinase gamma (PI3Kγ) inhibitor (PI), with surface modification using PCM peptide for cardiomyocyte-targeted delivery. In vitro and in vivo models of DIC were used to evaluate targeting specificity and therapeutic efficacy. Mechanistic investigations included ROS detection (DCFH-DA assay), inflammatory phenotype analysis (immunohistochemistry for CD68 and CD206), and autophagy flux assessment (immunofluorescence for LC3-II). Results: PGPP/NPs demonstrated selective accumulation in cardiomyocytes compared to non-targeted GPP/NPs (p<0.05). This nanocomposite significantly alleviated DIC through antioxidative, anti-inflammatory, and autophagy-promoting mechanisms. Notably, it reduced DIC severity while preserving the antitumor efficacy of DOX. Conclusion: This novel therapeutic strategy shows great promise for mitigating chemotherapy-induced cardiotoxicity and may be extended to other chemotherapeutic agents with cardiac side effects.
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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.