ArticleScientific reports2018
Intranasal Delivery of Copper Oxide Nanoparticles Induces Pulmonary Toxicity and Fibrosis in C57BL/6 mice.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
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Who cites it
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 147 citations in OpenAlex.
- Metal Nanoparticles in Infection and Immunity.Immunological investigations · 2020Pooled it
- Nrf2 pathway mediates copper oxide nanoparticle-induced exacerbation of allergic asthma.Redox biology · 2026Article
- Regulated Cell Death in Idiopathic Pulmonary Fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- Pulmonary Exposure to Copper Oxide Nanoparticles Induces Systemic Inflammation, Oxidative Stress, and Prothrombotic Responses in BALB/c Mice.International journal of nanomedicine · 2026Article
- Targeted drug delivery in neurodegenerative diseases: the role of nanotechnology.Frontiers in medicine · 2025Review
- Copper oxide nanoparticles exacerbate chronic obstructive pulmonary disease by activating the TXNIP-NLRP3 signaling pathway.Particle and fibre toxicology · 2024Article
- Copper Oxide Nanoparticles Induce Pulmonary Inflammation and Exacerbate Asthma via the TXNIP Signaling Pathway.International journal of molecular sciences · 2024Article
- Review
- MMP-3 mediates copper oxide nanoparticle-induced pulmonary inflammation and fibrosis.Journal of nanobiotechnology · 2024Article
- Nanoparticles and Airway Epithelial Cells: Exploring the Impacts and Methodologies in Toxicity Assessment.International journal of molecular sciences · 2024Review
- Copper homeostasis dysregulation in respiratory diseases: a review of current knowledge.Frontiers in physiology · 2024Review
- Toxicity of Metal Oxide Nanoparticles: Looking through the Lens of Toxicogenomics.International journal of molecular sciences · 2023Article
- Roles of Nrf2/HO-1 and ICAM-1 in the Protective Effect of Nano-Curcumin against Copper-Induced Lung Injury.International journal of molecular sciences · 2023Article
- MMP-3-mediated cleavage of OPN is involved in copper oxide nanoparticle-induced activation of fibroblasts.Particle and fibre toxicology · 2023Article
- Comparative Evaluation of the Cytotoxic Effects of Metal Oxide and Metalloid Oxide Nanoparticles: An Experimental Study.International journal of molecular sciences · 2023Article
- Early events marking lung fibroblast transition to profibrotic state in idiopathic pulmonary fibrosis.Respiratory research · 2023Article
- Comparative toxicological evaluations of novel forms nano-pesticides in liver and lung of albino rats.Journal of molecular histology · 2023Article
- Copper Exposure Induces Epithelial-Mesenchymal Transition-Related Fibrotic Change via Autophagy and Increase Risk of Lung Fibrosis in Human.Antioxidants (Basel, Switzerland) · 2023Article
- Recent advances in nanoparticle applications in respiratory disorders: a review.Frontiers in pharmacology · 2023Review
- Antimicrobial Properties of CuO Particles Deposited on a Medical Mask.Materials (Basel, Switzerland) · 2022Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Copper oxide nanoparticles (CuO NPs) are widely used as catalysts or semiconductors in material fields. Recent studies have suggested that CuO NPs have adverse genotoxicity and cytotoxicity effects on various cells. However, little is known about the toxicity of CuO NPs following exposure to murine lungs. The purpose of this fundamental research was to investigate whether CuO NPs could induce epithelial cell injury, pulmonary inflammation, and eventually fibrosis in C57BL/6 mice. Our studies showed that CuO NPs aggravated pulmonary inflammation in a dose-dependent manner. CuO NPs induced apoptosis of epithelial cells as indicated by TUNEL staining, flow cytometry and western blot analysis, which was partially caused by increased reactive oxygen species (ROS). In addition, CuO NPs exposure promoted collagen accumulation and expression of the progressive fibrosis marker α-SMA in the lung tissues, indicating that CuO NP inhalation could induce pulmonary fibrosis in C57BL/6 mice. All data provide novel evidence that there is an urgent need to prevent the adverse effects of CuO NPs in the human respiratory system.
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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.