ArticleToxicological sciences : an official journal of the Society of Toxicology2010
Acute cobalt-induced lung injury and the role of hypoxia-inducible factor 1alpha in modulating inflammation.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
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- A novel multifunctional fluorescent probe with ESIPT and AIE effects for the detection of CoRSC advances · 2025Article
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- Hypoxia-inducible factor (HIF)-1α-induced regulation of lung injury in pulmonary aspiration is mediated through NF-kB.FASEB bioAdvances · 2022Article
- Eosinophils, Hypoxia-Inducible Factors, and Barrier Dysfunction in Functional Dyspepsia.Frontiers in allergy · 2022Review
- SARS-CoV-2 infection causes prolonged cardiomyocyte swelling and inhibition of HIF1α translocation in an animal model COVID-19.Frontiers in cardiovascular medicine · 2022Article
- Adenosine at the Interphase of Hypoxia and Inflammation in Lung Injury.Frontiers in immunology · 2020Review
- Hypoxia-Inducible Factor (HIF)-1α Promotes Inflammation and Injury Following Aspiration-Induced Lung Injury in Mice.Shock (Augusta, Ga.) · 2019Article
- HIF-1α is a key mediator of the lung inflammatory potential of lithium-ion battery particles.Particle and fibre toxicology · 2019Article
- MicroRNA-21 Mediates the Protective Effects of Mesenchymal Stem Cells Derived from iPSCs to Human Bronchial Epithelial Cell Injury Under Hypoxia.Cell transplantation · 2018Article
- Contributions of nonhematopoietic cells and mediators to immune responses: implications for immunotoxicology.Toxicological sciences : an official journal of the Society of Toxicology · 2015Review
- Up-regulation of Gadd45α after exposure to metal nanoparticles: the role of hypoxia inducible factor 1α.Environmental toxicology · 2015Article
- Activation of hypoxia-inducible factor-1α in type 2 alveolar epithelial cell is a major driver of acute inflammation following lung contusion.Critical care medicine · 2014Article
- Loss of hypoxia-inducible factor 2 alpha in the lung alveolar epithelium of mice leads to enhanced eosinophilic inflammation in cobalt-induced lung injury.Toxicological sciences : an official journal of the Society of Toxicology · 2014Article
- Article
- Neonatal epithelial hypoxia inducible factor-1α expression regulates the response of the lung to experimental asthma.American journal of physiology. Lung cellular and molecular physiology · 2012Article
- The reaction of HOCl and cyanocobalamin: corrin destruction and the liberation of cyanogen chloride.Free radical biology & medicine · 2012Article
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8 authors at 4 institutions in 4 countries.
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Abstract
Air pollution is a critical factor in the development and exacerbation of pulmonary diseases. Ozone, automobile exhaust, cigarette smoke, and metallic dust are among the potentially harmful pollution components that are linked to disease progression. Transition metals, such as cobalt, have been identified at significant levels in air pollution. Cobalt exerts numerous biological effects, including mimicking hypoxia. Similar to hypoxia, cobalt exposure results in the stabilization of hypoxia-inducible factors (HIFs), a family of proteins that regulate the cellular response to oxygen deficit. HIFs also play an important role in innate immunity and inflammatory processes. To characterize the role of HIF1alpha, the most ubiquitously expressed HIF, in the early events during cobalt-induced lung inflammation, an inducible lung-specific HIF1alpha deletion model was employed. Control mice showed classical signs of metal-induced injury following cobalt exposure, including neutrophilic infiltration and induction of Th1 cytokines. In contrast, HIF1alpha-deficient mice exhibited pronounced eosinophil counts in bronchoalveolar lavage fluid and lung tissue complemented with Th2 cytokine induction. The timing of these results suggests that the loss of epithelial-derived HIF1alpha alters the lung's innate immune response and biases the tissue toward a Th2-mediated inflammation.
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