ArticleCell death & disease2017
Zinc oxide nanoparticles harness autophagy to induce cell death in lung epithelial cells.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 201 citations in OpenAlex.
- Mitochondrial Transport in Bone Metabolism Homeostasis: Molecular Mechanisms and Targeted Therapeutic Strategies.International journal of molecular sciences · 2026Review
- Metal-dependent regulated cell death: Molecular architecture and translational frontiers.iMeta · 2026Review
- Epithelial SLC39A1 prevents acute lung injury through zinc-mediated transcriptional activation of autophagy in male mice.Nature communications · 2026Article
- A multipurpose 1DZnO nanoplatform to combat ampicillin-resistant E. coli.Scientific reports · 2026Article
- Untargeted metabolomics reveals divergent metabolic profiles between the predatory Arma chinensis and the Phytophagous Halyomorpha halys.Journal of insect science (Online) · 2026Article
- Exposure to zinc oxide nanoparticles inhibits preimplantation embryonic development by disrupting zygotic genome activation.Cell biology and toxicology · 2025Article
- Extracellular Vesicles and Nanoparticles in Regenerative and Personalised Medicine: Diagnostic and Therapeutic Roles-A Narrative Review.Pharmaceutics · 2025Review
- Photodynamic Therapy for Glioblastoma: Potential Application of TiOPharmaceutics · 2025Review
- Rescuing lysosomal/autophagic defects via nanoapproach: implications for lysosomal/autophagic defect-related diseases.Journal of Zhejiang University. Science. B · 2025Review
- Biotechnological approaches and therapeutic potential of mitochondria transfer and transplantation.Nature communications · 2025Review
- An immune activator encapsulating PD-L1 siRNA for augmented immune checkpoint blockade immunotherapy through ZnJournal of nanobiotechnology · 2025Article
- Deciphering key nano-bio interface descriptors to predict nanoparticle-induced lung fibrosis.Particle and fibre toxicology · 2025Article
- Sustainable synthesis of zinc oxide nanoparticles fromFrontiers in molecular biosciences · 2025Article
- Reprogramming the tumor-immune landscape via nanomaterial-induced immunogenic cell death: a mini review.Frontiers in bioengineering and biotechnology · 2025Review
- Alveolar epithelial cell dysfunction and epithelial-mesenchymal transition in pulmonary fibrosis pathogenesis.Frontiers in molecular biosciences · 2025Review
- Mechanism of a Novel Complex: Zinc Oxide Nanoparticles-Luteolin to Promote Ferroptosis in Human Acute Myeloid Leukemia Cells in Vitro.International journal of nanomedicine · 2025Article
- Recent advances in nanoadjuvant-triggered STING activation for enhanced cancer immunotherapy.Heliyon · 2024Review
- Assessing the Toxicity of Metal- and Carbon-Based Nanomaterials In Vitro: Impact on Respiratory, Intestinal, Skin, and Immune Cell Lines.International journal of molecular sciences · 2024Article
- Cytotoxic Potencies of Zinc Oxide Nanoforms in A549 and J774 Cells.Nanomaterials (Basel, Switzerland) · 2024Article
- Nanotherapeutics targeting autophagy regulation for improved cancer therapy.Acta pharmaceutica Sinica. B · 2024Review
4 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although zinc oxide nanoparticles (ZnONPs) are widely used, they have raised concerns of toxicity in humans. Previous studies have indicated that reactive oxygen species (ROS) and autophagy are involved in the cytotoxicity of ZnONPs, but the regulatory mechanisms between autophagy and ROS remain to be elucidated. Herein, we comprehensively investigated the regulatory mechanism of autophagy and the link between autophagy and ROS in ZnONPs-treated lung epithelial cells. We demonstrated that ZnONPs could induce autophagy, and this process could enhance the dissolution of ZnONPs in lysosomes to release zinc ions. Sequentially, zinc ions released from ZnONPs were able to damage not only lysosomes, leading to impaired autophagic flux, but also mitochondria. Impaired autophagic flux resulted in the accumulation of damaged mitochondria, which could generate excessive ROS to cause cell death. We further demonstrated that the inhibition of autophagy by either pharmacological inhibitors or small interfering RNA (siRNA)-mediated knockdown of Beclin-1 and AMP-activated protein kinase could ameliorate ZnONPs-induced cell death. Moreover, we found that lysosomal-associated membrane protein 1/2 (LAMP-1/2), which were the most abundant highly glycosylated protein in late endosomes/lysosomes, exhibited aberrant expression pattern upon treatment with ZnONPs. Intriguingly, LAMP-2 knockdown, but not LAMP-1 knockdown, could exacerbate the ROS generation and cell death induced by ZnONPs treatment. Meanwhile, LAMP-2 overexpression alleviated ZnONPs-induced cell death, suggesting that LAMP-2 was linked to this toxic phenotype induced by ZnONPs. Our results indicate that autophagic dysfunction could contribute to excessive ROS generation upon treatment with ZnONPs in lung epithelial cells, suggesting that modulating the autophagy process would minimize ZnONPs-associated toxicity.
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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.