ArticlePhysiological reports2016
Low-dose oral cadmium increases airway reactivity and lung neuronal gene expression in mice.
Article in Physiological reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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
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Who cites it
19 citing papers in PubMed, 41 citations in OpenAlex.
- Single-cell RNA sequencing reveals dysregulation of innate immune signaling in early-life respiratory syncytial virus infection with subsequent low-level cadmium exposure.Toxicology reports · 2026Article
- The effects of combined low-dose cadmium and deltamethrin on mitochondrial bioenergetics and metabolism in human lung fibroblasts.Toxicology reports · 2025Article
- Cadmium exposure following early-life respiratory syncytial virus infection promotes lung fibrosis through autophagy inhibition.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- Ellagic Acid Reduces Cadmium Exposure-Induced Apoptosis in HT22 Cells via Inhibiting Oxidative Stress and Mitochondrial Dysfunction and Activating Nrf2/HO-1 Pathway.Antioxidants (Basel, Switzerland) · 2024Article
- Pyrimidine Biosynthesis in Branching Morphogenesis Defects Induced by Prenatal Heavy Metal Exposure.American journal of respiratory cell and molecular biology · 2024Article
- Heavy Metal Exposure-Mediated Dysregulation of Sphingolipid Metabolism.Antioxidants (Basel, Switzerland) · 2024Article
- A hypothesis: Potential contributions of metals to the pathogenesis of pulmonary artery hypertension.Life sciences · 2024Review
- Study on the relationship between selenium and cadmium in diseased human lungs.Advances in redox research · 2023Article
- Low-Dose Cadmium Potentiates Metabolic Reprogramming Following Early-Life Respiratory Syncytial Virus Infection.Toxicological sciences : an official journal of the Society of Toxicology · 2022Article
- Review
- Environmental Cadmium Enhances Lung Injury by Respiratory Syncytial Virus Infection.The American journal of pathology · 2019Article
- Low-dose cadmium potentiates lung inflammatory response to 2009 pandemic H1N1 influenza virus in mice.Environment international · 2019Article
- Redox Systems Biology of Nutrition and Oxidative Stress.The Journal of nutrition · 2019Article
- Low-dose cadmium disrupts mitochondrial citric acid cycle and lipid metabolism in mouse lung.Free radical biology & medicine · 2019Article
- Selenium supplementation prevents metabolic and transcriptomic responses to cadmium in mouse lung.Biochimica et biophysica acta. General subjects · 2018Article
- Selenium at the redox interface of the genome, metabolome and exposome.Free radical biology & medicine · 2018Review
- Low-dose cadmium exposure induces peribronchiolar fibrosis through site-specific phosphorylation of vimentin.American journal of physiology. Lung cellular and molecular physiology · 2017Article
- Article
- Low-dose oral cadmium increases airway reactivity and lung neuronal gene expression in mice.Physiological reports · 2016Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Inhalation of cadmium (Cd) is associated with lung diseases, but less is known concerning pulmonary effects of Cd found in the diet. Cd has a decades-long half-life in humans and significant bioaccumulation occurs with chronic dietary intake. We exposed mice to low-dose CdCl2 (10 mg/L in drinking water) for 20 weeks, which increased lung Cd to a level similar to that of nonoccupationally exposed adult humans. Cd-treated mice had increased airway hyperresponsiveness to methacholine challenge, and gene expression array showed that Cd altered the abundance of 443 mRNA transcripts in mouse lung. In contrast to higher doses, low-dose Cd did not elicit increased metallothionein transcripts in lung. To identify pathways most affected by Cd, gene set enrichment of transcripts was analyzed. Results showed that major inducible targets of low-dose Cd were neuronal receptors represented by enriched olfactory, glutamatergic, cholinergic, and serotonergic gene sets. Olfactory receptors regulate chemosensory function and airway hypersensitivity, and these gene sets were the most enriched. Targeted metabolomics analysis showed that Cd treatment also increased metabolites in pathways of glutamatergic (glutamate), serotonergic (tryptophan), cholinergic (choline), and catecholaminergic (tyrosine) receptors in the lung tissue. Protein abundance measurements showed that the glutamate receptor GRIN2A was increased in mouse lung tissue. Together, these results show that in mice, oral low-dose Cd increased lung Cd to levels comparable to humans, increased airway hyperresponsiveness and disrupted neuronal pathways regulating bronchial tone. Therefore, dietary Cd may promote or worsen airway hyperresponsiveness in multiple lung diseases including asthma.
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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.