ArticleToxicology letters2016
Transient receptor potential (TRP) channels as a therapeutic target for intervention of respiratory effects and lethality from phosgene.
Article in Toxicology letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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Who cites it
9 citing papers in PubMed, 20 citations in OpenAlex.
- Phosgene inhalation injury in mice: Modeling human pathophysiology, biomarker discovery, and therapeutic target identification.Toxicology and applied pharmacology · 2026Article
- Claudin and transmembrane receptor protein gene expressions are reversely correlated in peritumoral brain edema.Cancer medicine · 2024Article
- Mechanism of Phosgene-Induced Acute Lung Injury and Treatment Strategy.International journal of molecular sciences · 2021Review
- Toxic effects of chlorine gas and potential treatments: a literature review.Toxicology mechanisms and methods · 2021Review
- Transient receptor potential channels in pulmonary chemical injuries and as countermeasure targets.Annals of the New York Academy of Sciences · 2020Article
- Mibefradil and Flunarizine, Two T-Type Calcium Channel Inhibitors, Protect Mice against Lipopolysaccharide-Induced Acute Lung Injury.Mediators of inflammation · 2020Article
- Transient Receptor Potential Ion Channel-Dependent Toxicity of Silica Nanoparticles and Poly(amido amine) Dendrimers.The Journal of pharmacology and experimental therapeutics · 2019Article
- Review
- Phosgene-induced acute lung injury (ALI): differences from chlorine-induced ALI and attempts to translate toxicology to clinical medicine.Clinical and translational medicine · 2017Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Phosgene (CG), a toxic inhalation and industrial hazard, causes bronchoconstriction, vasoconstriction and associated pathological effects that could be life threatening. Ion channels of the transient receptor potential (TRP) family have been identified to act as specific chemosensory molecules in the respiratory tract in the detection, control of adaptive responses and initiation of detrimental signaling cascades upon exposure to various toxic inhalation hazards (TIH); their activation due to TIH exposure may result in broncho- and vasoconstriction. We studied changes in the regulation of intracellular free Ca(2+) concentration ([Ca(2+)]i) in cultures of human bronchial smooth muscle cells (BSMC) and human pulmonary microvascular endothelial cells (HPMEC) exposed to CG (16ppm, 8min), using an air/liquid interface exposure system. CG increased [Ca(2+)]i (p<0.05) in both cell types, The CG-induced [Ca(2+)]i was blocked (p<0.05) by two types of TRP channel blockers, SKF-96365, a general TRP channel blocker, and RR, a general TRPV (vanilloid type) blocker, in both BSMC and HPMEC. These effects correlate with the in vivo efficacies of these compounds to protect against lung injury and 24h lethality from whole body CG inhalation exposure in mice (8-10ppm×20min). Thus the TRP channel mechanism appears to be a potential target for intervention in CG toxicity.
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Registered trials
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