ArticleJournal of nanobiotechnology2022
Ceria-Zirconia nanoparticles reduce intracellular globotriaosylceramide accumulation and attenuate kidney injury by enhancing the autophagy flux in cellular and animal models of Fabry disease.
Article in Journal of nanobiotechnology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Nanotechnology-mediated podocyte injury repair: mechanistic exploration and therapeutic prospects.Renal failure · 2026Review
- Pathophysiological mechanisms of organ injury in Fabry disease: Update via multi-omics.Genes & diseases · 2026Review
- Modeling Fabry nephropathy: insights from experimental systems towards precision nephrology.Disease models & mechanisms · 2026Review
- Lysosomal checkpoints in renal autoimmunity: from antigen processing to metabolic-immune crosstalk.Frontiers in immunology · 2026Review
- Zirconium-Doped Ceria Oxide Nanozymes Alleviate Allergic Rhinitis by Attenuating Oxidative Stress and Stabilizing Mast Cells.International journal of nanomedicine · 2026Article
- Mechanisms and Therapeutic Perspectives of Podocyte Aging in Podocytopathies.International journal of molecular sciences · 2025Review
- Autolysosomal Dysfunction in Obesity-induced Metabolic Inflammation and Related Disorders.Current obesity reports · 2025Review
- PEG-Coated Ceria-Zirconia Nanoparticle Prevent Weight Gain and Obesity-Related Organ Damage Through Autophagy Flux Activation and ROS Scavenging.International journal of nanomedicine · 2025Article
- Zirconia/dental pulp stem cell composite scaffolds repair osteogenic defect via regulating macrophages.Frontiers in bioengineering and biotechnology · 2025Article
- The impact of nanomaterials on autophagy across health and disease conditions.Cellular and molecular life sciences : CMLS · 2024Review
- Autophagy-modulating biomaterials: multifunctional weapons to promote tissue regeneration.Cell communication and signaling : CCS · 2024Review
- The role of tubular cells in the pathogenesis of Fabry nephropathy.Frontiers in cardiovascular medicine · 2024Review
- Engineering antioxidant ceria-zirconia nanomedicines for alleviating podocyte injury in rats with adriamycin-induced nephrotic syndrome.Journal of nanobiotechnology · 2023Article
- Biochemical Mechanisms beyond Glycosphingolipid Accumulation in Fabry Disease: Might They Provide Additional Therapeutic Treatments?Journal of clinical medicine · 2023Review
- Salvianolic acid B attenuates membranous nephropathy by activating renal autophagy via microRNA-145-5p/phosphatidylinositol 3-kinase/AKT pathway.Bioengineered · 2022Article
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15 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundFabry disease (FD) is a lysosome storage disease (LSD) characterized by significantly reduced intracellular autophagy function. This contributes to the progression of intracellular pathologic signaling and can lead to organ injury. Phospholipid-polyethyleneglycol-capped Ceria-Zirconia antioxidant nanoparticles (PEG-CZNPs) have been reported to enhance autophagy flux. We analyzed whether they suppress globotriaosylceramide (Gb3) accumulation by enhancing autophagy flux and thereby attenuate kidney injury in both cellular and animal models of FD.
resultsGb3 was significantly increased in cultured human renal proximal tubular epithelial cells (HK-2) and human podocytes following the siRNA silencing of α galactosidase A (α-GLA). PEG-CZNPs effectively reduced the intracellular accumulation of Gb3 in both cell models of FD and improved both intracellular inflammation and apoptosis in the HK-2 cell model of FD. Moreover these particles attenuated pro fibrotic cytokines in the human podocyte model of FD. This effect was revealed through an improvement of the intracellular autophagy flux function and a reduction in reactive oxygen species (ROS). An FD animal model was generated in which 4-week-old male B6;129-Gla
conclusionsPEG-CZNPs alleviate FD associated kidney injury by enhancing autophagy function and thus provide a foundation for the development of new drugs to treat of storage disease.
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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.