ArticleCell communication and signaling : CCS2024
Cadmium exposure triggers alveolar epithelial cell pyroptosis by inducing mitochondrial oxidative stress and activating the cGAS-STING pathway.
Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed.
- Radiotherapy-Induced Side Effects: Epidemiology, Pathogenesis, Prevention and Treatments.MedComm · 2026Review
- Nifuroxazide Pretreatment Protects Against Acute CdClAntioxidants (Basel, Switzerland) · 2026Article
- Tanshinone IIA Attenuates Pulmonary Fibrosis via Dual Inhibition of JNK and Smad Signaling.Antioxidants (Basel, Switzerland) · 2026Article
- Biochanin-A, Coenzyme Q10, and Phloretin Mitigate Cadmium-Induced Pulmonary and Testicular Toxicity in Mice Through Modulating Oxidative Stress and Apoptosis Via SIRT1-NRF2-KEAP1 Signaling Pathway.Biological trace element research · 2026Article
- Fibroblast growth factor-inducible 14 accelerates pulmonary fibrosis by inducing fibroblast senescence in mice.Cellular and molecular life sciences : CMLS · 2026Article
- cGAS-STING signaling in pollution-induced toxicity: mechanism and relieving medication.Apoptosis : an international journal on programmed cell death · 2026Review
- Impaired BCAA Catabolism Contributes To Acute Lung Injury By Triggering Oxidative Stress and Inflammatory Response Via the MAPK Pathway.Inflammation · 2026Article
- Depleted uranium exposure induced ferroptosis in renal cells via the ETHE1/P38-MAPK pathway.Archives of toxicology · 2026Article
- The cGAS-STING pathway and mitochondrial metabolism: from mechanistic insights to therapeutic potential in tumor.Journal of translational medicine · 2026Review
- The cGAS-STING pathway in pulmonary infectious and sterile inflammation: differences, connections, and therapeutic implications.Frontiers in immunology · 2026Review
- Research progress on molecular mechanisms and signaling pathways of toxic metal exposure-induced lung fibrosis.Frontiers in immunology · 2026Review
- Neurotoxic mechanisms of cadmium in neurodegenerative diseases.Frontiers in cell and developmental biology · 2026Review
- Protective effects of human umbilical cord mesenchymal stem cells-derived small extracelluar vesicles on corneal epithelial cells under hyperosmotic stress: Inhibition of oxidative damage and inflammation.Genetics and molecular biology · 2026Article
- PDHA1 Hyperactivation Orchestrates Metabolic Reprogramming Promoting Endothelial Senescence.Research (Washington, D.C.) · 2026Article
- Association between heavy metal exposure and chronic cough: the mediating roles of inflammation.Annals of medicine · 2025Article
- Dietary influence on lung injury and immune modulation in cadmium-exposed mice.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- The predictive value of multiple urinary metals in evaluating death risk in asthmatic individuals: a prospective cohort study.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2025Article
- Review
- Diverse functions of NLRP3 inflammasome in PANoptosis and diseases.Cell death discovery · 2025Review
- Epitranscriptomic alterations induced by environmental toxins: implications for RNA modifications and disease.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2025Review
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Authors and funding
9 authors.
Funding
Abstract
backgroundCadmium is a ubiquitous toxic metal and environmental pollutant. More and more studies have shown that cadmium exposure can damage lung function. Alveolar epithelial cells (AECs) are structural cells that maintain the stability of lung function. The injury of AECs is an essential determinant of many lung diseases. In the lung, cadmium accumulation can cause damage to AECs. However, the specific mechanism is still unclear. This study aimed to explore the key mechanism underlying the injury of AECs caused by cadmium exposure.
methodsThe main modes of death of AECs induced by cadmium exposure were evaluated in vivo and in vitro. Transcriptomic changes of AECs induced by cadmium exposure were analyzed using RNA-sequence. Mitochondrial ROS scavengers (mitoQ), voltage-dependent anion channel 1 (VDAC1) oligomer inhibitor (VBIT4), and cyclic GMP-AMP synthase (cGAS) inhibitor (RU.521) were used to assess whether cadmium exposure triggered pyroptosis of AECs by inducing mitochondrial stress to activate the cGAS-STING-NLRP3 axis.
resultsIn this study, the expression of pyroptosis-related proteins was significantly up-regulated in the cadmium-exposed AECs, while the expression of apoptosis, necroptosis, and ferroptosis-related proteins had no significant up-regulated. The pan-caspase inhibitor ZVAD-FMK significantly reduced cell death. Thus, our research indicates that pyroptosis is the primary type of AEC death exported to cadmium. Mechanistically, RNA-seq and Western Blot results showed that cadmium exposure activated the cGAS-STING pathway in AECs and promoted pyroptosis by activating the NLRP3 inflammasome. Further investigation of the mechanism found that cadmium exposure caused mitochondrial oxidative stress, which led to mtDNA leakage into the cytoplasm and activated the cGAS-STING pathway. In addition, inhibition of the cGAS-STING pathway significantly alleviated lung injury induced by cadmium exposure in mice.
conclusionOur study confirmed that pyroptosis of AECs was a vital mechanism of lung injury after cadmium exposure in a cGAS-STING-dependent manner, which may provide a new target for the treatment of lung diseases induced by cadmium exposure.
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