ArticleJournal of nanobiotechnology2025
HPDA-based tubule-targeting nanoplatform alleviates oxidative stress and ferroptosis for the reversal of renal interstitial fibrosis.
Article in Journal of nanobiotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Regulated cell death: a multidimensional regulatory network in the pathogenesis of renal fibrosis.Apoptosis : an international journal on programmed cell death · 2026Review
- The Mechanism and Application of Traditional Chinese Medicine Nano-Formulations in the Treatment of Renal Fibrosis.International journal of nanomedicine · 2026Review
- Engineering Kidney-Targeted Drug Delivery Systems: Principles, Materials, and Emerging Strategies.International journal of nanomedicine · 2026Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
backgroundRenal interstitial fibrosis (RIF) is a hallmark pathological process in the progression of chronic kidney disease (CKD). However, effective therapies to halt or reverse RIF remain limited. Emerging evidence implicates ferroptosis as a critical contributor to RIF. Rosiglitazone (Rosi), a widely used thiazolidinedione, exhibits anti-ferroptotic activity but suffers from poor aqueous solubility, limited renal specificity, and systemic side effects.
resultsHere, we constructed a renal tubular epithelial cell-targeted nano-based drug delivery system-Rosi-loaded, K3 peptide-modified, PEGylated hollow polydopamine(HPDA) nanoparticles (Rosi@HPDA-PEG-K3 NPs). This system displayed excellent biocompatibility and lesion-specific targeting, achieving prolonged retention in fibrotic kidneys. The in vitro and in vivo experiment demonstrated that this nano-based drug delivery system inhibited ferroptosis through downregulation of ACSL4, iron ion chelation, and ROS scavenging. Concurrently, it stabilized mitochondrial membrane potential and synergistically suppressed inflammatory responses, ultimately attenuating RIF.
conclusionsIn summary, Rosi@HPDA-PEG-K3 NPs deliver Rosi specifically to renal renal tubular epithelial cells(TECs)and exert an anti-RIF effect through the integration of ferroptosis inhibition, mitochondrial protection, and inflammation modulation. Our study establishes a nanotherapeutic platform with precise targeting and multifunctional efficacy, highlighting its scientific rigor and the clinical translational potential of RIF.
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