ArticleEnvironmental science and pollution research international2018
Nickle(II) ions exacerbate bleomycin-induced pulmonary inflammation and fibrosis by activating the ROS/Akt signaling pathway.
Article in Environmental science and pollution research international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 31 citations in OpenAlex.
- Comparative study on mouse models of acute exacerbation of pulmonary fibrosis.Experimental and therapeutic medicine · 2026Article
- Metalloimmunotherapies: metal-driven regulatory networks in the immune microenvironment.Frontiers in immunology · 2026Review
- Molecular Hydrogen Ameliorates Anti-Desmoglein 1 Antibody-Induced Pemphigus-Associated Interstitial Lung Disease by Inhibiting Oxidative Stress.International journal of molecular sciences · 2025Article
- Current advancements in the mechanisms and animal models of acute exacerbation of pulmonary fibrosis: a systematic review.Frontiers in pharmacology · 2025Review
- Exploring Associations and Mediating Factors between Multiple Trace Metals with Anemia in US Adults: Insight from NHANES 2017-2020.Nutrients · 2024Article
- Animal models of acute exacerbation of pulmonary fibrosis.Respiratory research · 2023Review
- Histone deacetylase 3 deletion in alveolar type 2 epithelial cells prevents bleomycin-induced pulmonary fibrosis.Clinical epigenetics · 2023Article
- Coal dust nanoparticles induced pulmonary fibrosis by promoting inflammation and epithelial-mesenchymal transition via the NF-κB/NLRP3 pathway driven by IGF1/ROS-mediated AKT/GSK3β signals.Cell death discovery · 2022Article
- PM2.5 Exposure Induces Lung Injury and Fibrosis by Regulating FerroptosisDisease markers · 2022Article
- Epigallocatechin Gallate Relieved PM2.5-Induced Lung Fibrosis by Inhibiting Oxidative Damage and Epithelial-Mesenchymal Transition through AKT/mTOR Pathway.Oxidative medicine and cellular longevity · 2022Article
- Study on Lung Injury Caused by Fine Particulate Matter and Intervention Effect ofEvidence-based complementary and alternative medicine : eCAM · 2022Article
- Evaluation of the effect of filtered ultrafine particulate matter on bleomycin-induced lung fibrosis in a rat model using computed tomography, histopathologic analysis, and RNA sequencing.Scientific reports · 2021Article
- Combined Toxicity of Metal Nanoparticles: Comparison of Individual and Mixture Particles Effect.Advances in experimental medicine and biology · 2021Article
- Small GTPase RAB6 deficiency promotes alveolar progenitor cell renewal and attenuates PM2.5-induced lung injury and fibrosis.Cell death & disease · 2020Article
- Extracellular Vesicles Derived from Adipose Mesenchymal Stem Cells Alleviate PM2.5-Induced Lung Injury and Pulmonary Fibrosis.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- PMFrontiers in physiology · 2019Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Nickle (Ni) is a heavy metal found in particulate matter. We previously reported that Ni ions are strongly associated with high apoptosis rates and high expression of IL-1β in human bronchial epithelial cells following exposure to PM2.5; however, the effects of Ni ions on pulmonary fibrosis have not been fully elucidated. In the current study, we evaluated whether Ni ions can exacerbate bleomycin (BLM)-induced pulmonary fibrosis in a mouse model and illustrated the potential mechanism. Ni ions inhibited cell proliferation and induced apoptosis in A549 and MRC-5 cells. BLM-induced lung injury and fibrosis in mice were significantly enhanced by nickel treatment, and these findings were also supported by inflammatory cell accumulation in bronchoalveolar lavage fluid and elevated levels of pro-inflammatory cytokines in lung tissues. Ni ions also increased extracellular matrix protein levels, including those of type I collagen and MMP9 in mouse lung tissues and cell lines. Moreover, Ni ions promoted the phosphorylation of AKT in this mouse model. The effect of increased collagen levels and MMP9 expression was inhibited by blocking the AKT phosphorylation. Together, these findings suggest AKT activation as a critical contributor to this Ni-exacerbated pulmonary fibrotic process.
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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.