ArticleThe Journal of biological chemistry2020
Cadmium-mediated lung injury is exacerbated by the persistence of classically activated macrophages.
Article in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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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.
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- Breathing lung-on-chip: a versatile tool for assessing respiratory toxicity across multiple therapeutic modalities.Archives of toxicology · 2026Article
- Toward Smart Salivary Diagnostics: A Comprehensive Review of Heavy Metal Biomarkers and Digital Risk Modeling.Diagnostics (Basel, Switzerland) · 2026Review
- Review
- Dietary influence on lung injury and immune modulation in cadmium-exposed mice.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Intracellular methylglyoxal accumulation in classically activated mouse macrophages is mediated by HIF-1α.Journal of leukocyte biology · 2025Article
- Heavy metals: toxicity and human health effects.Archives of toxicology · 2025Review
- The Protective Effects ofToxics · 2024Article
- Cadmium-induced lung injury is associated with oxidative stress, apoptosis, and altered SIRT1 and Nrf2/HO-1 signaling; protective role of the melatonin agonist agomelatine.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Myeloid Heterogeneity Mediates Acute Exacerbations of Pulmonary Fibrosis.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Article
- Disease-associated metabolic pathways affected by heavy metals and metalloid.Toxicology reports · 2023Review
- Immunostimulatory and anti-inflammatory impact ofFrontiers in immunology · 2023Article
- Korean Red Ginseng water extract inhibits cadmium-induced lung injury via suppressing MAPK/ERK1/2/AP-1 pathway.Journal of ginseng research · 2022Article
- Inflammation resolution in environmental pulmonary health and morbidity.Toxicology and applied pharmacology · 2022Review
- Can PPARBiomolecules · 2022Article
- Use of Generalized Weighted Quantile Sum Regressions of Tumor Necrosis Factor Alpha and Kidney Function to Explore Joint Effects of Multiple Metals in Blood.International journal of environmental research and public health · 2022Article
- Cadmium Body Burden and Inflammatory Arthritis: A Pilot Study in Patients from Lower Silesia, Poland.International journal of environmental research and public health · 2022Article
- The function of omega-3 polyunsaturated fatty acids in response to cadmium exposure.Frontiers in immunology · 2022Review
- Cadmium and wild boar: Environmental exposure and immunological impact on macrophages.Toxicology reports · 2022Article
- Vanillin Attenuates Cadmium-Induced Lung Injury Through Inhibition of Inflammation and Lung Barrier Dysfunction Through Activating AhR.Inflammation · 2021Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Heavy metals released into the environment have a significant effect on respiratory health. Lung macrophages are important in mounting an inflammatory response to injury, but they are also involved in repair of injury. Macrophages develop mixed phenotypes in complex pathological conditions and polarize to a predominant phenotype depending on the duration and stage of injury and/or repair. Little is known about the reprogramming required for lung macrophages to switch between these divergent functions; therefore, understanding the mechanism(s) by which macrophages promote metabolic reprogramming to regulate lung injury is essential. Here, we show that lung macrophages polarize to a pro-inflammatory, classically activated phenotype after cadmium-mediated lung injury. Because metabolic adaptation provides energy for the diverse macrophage functions, these classically activated macrophages show metabolic reprogramming to glycolysis. RNA-Seq revealed up-regulation of glycolytic enzymes and transcription factors regulating glycolytic flux in lung macrophages from cadmium-exposed mice. Moreover, cadmium exposure promoted increased macrophage glycolytic function with enhanced extracellular acidification rate, glycolytic metabolites, and lactate excretion. These observations suggest that cadmium mediates the persistence of classically activated lung macrophages to exacerbate lung injury.
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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.