ArticleRegenerative therapy2025
Iron-Quercetin complex enhances mesenchymal stem cell-mediated HGF secretion and c-Met activation to ameliorate acute kidney injury through the prevention of tubular cell apoptosis.
Article in Regenerative therapy, 2025. 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.
- Targeting cellular senescence in diabetic kidney disease: potential of regenerative, cell-based therapies and other senotherapeutic approaches.Kidney international · 2026Review
- Iron-quercetin nanocomplex preconditioning reprograms the mesenchymal stem cell secretome to drive angiogenic, fibroblast and immunoregulatory wound repair.Regenerative biomaterials · 2026Article
- Advancing mesenchymal stem cell therapy for kidney diseases in companion animals: from mechanisms to clinical application.Frontiers in veterinary science · 2026Review
- Characterization of PBMC secretome: Iron-quercetin preconditioning enhances pro-angiogenic and tissue regeneration factors for potential autologous diabetic wound healing applications.Biochemistry and biophysics reports · 2025Article
- The Role of Viral Infections in Acute Kidney Injury and Mesenchymal Stem Cell-Based Therapy.Stem cell reviews and reports · 2025Review
- Non-hormone replacement therapy to overcome premature ovarian insufficiency: advances in natural products and stem cells targeting autophagy.Frontiers in endocrinology · 2025Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Acute kidney injury (AKI) is a life-threatening clinical syndrome with no effective treatment currently available. This study aims to investigate whether Iron-Quercetin complex (IronQ) pretreatment can enhance the therapeutic efficacy of Mesenchymal stem cells (MSCs) in AKI and explore the underlying mechanisms. Methods: A cisplatin-induced AKI model was established in male C57BL/6 mice, followed by the intravenous administration of 1x10ˆ6 MSCs or IronQ-pretreated MSCs (MSC Results: Compared to MSC-treated AKI mice, those treated with MSC Conclusions: IronQ pretreatment enhances MSCs efficacy in AKI by promoting HGF expression and secretion, activating the HGF/c-Met pathway to suppress tubular cell apoptosis. These findings indicate that IronQ improves MSC-based therapies and offers insights into molecular mechanisms, supporting the development of better AKI treatments.
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Registered trials
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