ArticleJournal of nanobiotechnology2021
Autophagy deficiency exacerbates acute lung injury induced by copper oxide nanoparticles.
Article in Journal of nanobiotechnology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 36 citations in OpenAlex.
- Sulfhydrated TFEB alleviates blast-induced lung injury by maintaining epithelial barrier integrity through the IGF2R/MMP-2/9 pathway.Redox biology · 2026Article
- Epithelial SLC39A1 prevents acute lung injury through zinc-mediated transcriptional activation of autophagy in male mice.Nature communications · 2026Article
- Pulmonary Exposure to Copper Oxide Nanoparticles Induces Systemic Inflammation, Oxidative Stress, and Prothrombotic Responses in BALB/c Mice.International journal of nanomedicine · 2026Article
- A Comprehensive Review on Copper Oxide Nanoparticles: Physicochemical Parameters, Pharmacological Potential and Pathophysiological Effects.International journal of nanomedicine · 2026Review
- Copper Oxide Nanoparticles Induce Pulmonary Inflammation and Exacerbate Asthma via the TXNIP Signaling Pathway.International journal of molecular sciences · 2024Article
- Inhalation exposure-induced toxicity and disease mediated via mTOR dysregulation.Experimental biology and medicine (Maywood, N.J.) · 2024Review
- Mitochondrial pathways of copper neurotoxicity: focus on mitochondrial dynamics and mitophagy.Frontiers in molecular neuroscience · 2024Review
- Nickel nanoparticles induce autophagy and apoptosis via HIF-1α/mTOR signaling in human bronchial epithelial cells.Environmental pollution (Barking, Essex : 1987) · 2023Article
- Mechanisms of cell injury induced by inhaled molybdenum trioxide nanoparticles in Golden Syrian Hamsters.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- Reciprocal regulation of NRF2 by autophagy and ubiquitin-proteasome modulates vascular endothelial injury induced by copper oxide nanoparticles.Journal of nanobiotechnology · 2022Article
- PINK1/TAX1BP1-directed mitophagy attenuates vascular endothelial injury induced by copper oxide nanoparticles.Journal of nanobiotechnology · 2022Article
- Electroacupuncture Preconditioning Alleviates Lipopolysaccharides-Induced Acute Lung Injury by Downregulating LC3-II/I and Beclin 1 Expression.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- The Molecular Mechanisms of Defective Copper Metabolism in Diabetic Cardiomyopathy.Oxidative medicine and cellular longevity · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
Copper oxide nanoparticles (CuONPs) are one of the widely used metal nanoparticles in the industrial and commercial fields. Autophagy is an intracellular degradation system that delivers cytoplasmic constituents to the lysosome and has been linked to nanoparticles-induced toxicity. In particular, the roles of autophagy in response to CuONPs have been explored in vitro, although the conclusions are controversial. To clarify the role of autophagy in CuONPs-induced acute lung injury, microtubule-associated protein 1 light chain 3 beta (Map1lc3b or lc3b) knockout mice and their corresponding wild type mice are applied. Our results showed that single-dose intratracheal instillation of CuONPs with dosages of 1.25, 2.5 or 5 mg/kg caused acute lung injury 3 days after treatment in a dose-dependent manner, as evidenced by deteriorative lung histopathology, more infiltration of macrophage cells, increased oxidative stress and copper ions. Loss of lc3b resulted in aggravated lung injury induced by CuONPs, which was probably due to the blockade of mitophagy and consequently the accumulation of aberrant mitochondria with overloaded copper ions. Our study provides the first in vivo evidence that autophagy deficiency exacerbates CuONPs-induced acute lung injury, and highlights that targeting autophagy is a meaningful strategy against CuONPs-associated respiratory toxicity.
Indexed as
Identifiers
What OpenQuestion holds
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.