ArticleTheranostics2025
Targeting granulosa cells with engineered DFO nanoparticles for the treatment of chemotherapy-induced premature ovarian failure.
Article in Theranostics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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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
10 citing papers in PubMed.
- Modern Polycystic Ovary Syndrome (PCOS) Management: Intelligent Drug Delivery and Metabolic Reprogramming for Ovarian Restoration and Fertility Optimization.Biomolecules · 2026Review
- Relationship between different modes of death and premature ovarian insufficiency: a literature review.Apoptosis : an international journal on programmed cell death · 2026Review
- Article
- Ferroptosis-autophagy crosstalk in bladder cancer: mechanisms and therapeutic implications.Molecular cancer · 2026Review
- HuMSCs-derived exosomes alleviate premature ovarian insufficiency by enhancing SIRT3-mediated mitochondrial function in theca-interstitial cells.Journal of ovarian research · 2026Article
- From gut-reproductive microbiota to ferroptosis: a comprehensive insight into the molecular-pathogenicity of endometriosis.Frontiers in immunology · 2026Review
- Inflammatory remodeling of the ovarian microenvironment in premature ovarian insufficiency: mechanisms and therapeutic opportunities.Frontiers in immunology · 2026Review
- Biomaterials for Reproductive Restoration: Translating Engineering Innovations.Biomaterials research · 2026Review
- Pyroptosis in premature ovarian insufficiency: pathogenic mechanisms, pathway crosstalk, and therapeutic strategies.Frontiers in medicine · 2026Review
- A Two-Hit Hypothesis for Chemotherapy-Induced Primary Ovarian Insufficiency in Asian Populations: A Population-Specific Mechanistic Framework Linking Genetic Susceptibility and Cytotoxic Stress via the PI3K-AKT-FOXO3 Axis.BioMed research international · 2026Review
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Premature ovarian failure (POF) is a prevalent and lethal adverse event that severely affects female cancer patients receiving chemotherapy. It is highly correlated with the collateral damage to ovarian granulosa cells caused by ferroptosis. The excessive iron accumulation in the intracellular labile iron pool (LIP) and the aberrant generation of reactive oxygen species (ROS) is the major cause of ferroptosis. No compounds with both ferroptosis inhibition functions and ovarian-targeting specificity that do not reduce systemic chemotherapeutic efficacy have been successful in treating the POF in the clinic trials. We herein in report a multifunctional FSH-mPDA@DFO nanoparticle that can prevent chemotherapy-induced DFO by targeting LIP and ROS to restrict ferroptosis. The FSH-mPDA@DFO are constructed by encapsulating deferoxamine (DFO) within mesoporous polydopamine nanoparticles conjugated with an ovarian granulosa cell-targeting peptide (FSHβ). They downregulate transferrin receptor (TFRC) expression, reduce cellular iron ion uptake, and inhibit ferritinophagy-mediated iron mobilization, thereby ameliorating LIP overload and regulating iron metabolism. More importantly, FSH-mPDA@DFO nanoparticles can specifically accumulate in the mitochondria and suppress excessive mitophagy to preserve mitochondrial integrity and attenuate iron release and ROS generation.
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