ArticleResearch square2025
The Functionality of the Cysteinyl Leukotriene Receptor 1 (CysLTR1) in the Lung by Metabolomics Analysis of Bronchoalveolar Lavage Fluid.
Article in Research square, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
- Updated by
Authors and funding
4 authors.
Funding
Abstract
Introduction: The cysteinyl leukotriene receptor 1 (CysLTR1) is known as a potent lipid mediator with a well-established role in inflammatory regulation and lung disease. While its involvement in immune cell recruitment has been previously reported, its broader impact on pulmonary metabolism remains poorly understood. Objectives: The study aims to investigate the metabolic consequences of a CysLTR1 deletion in mice to elucidate its role in pulmonary metabolic homeostasis. Methods: Bronchoalveolar lavage fluid (BALF) was collected from CysLTR1 knockout (KO) and wild-type (WT) mice and analysed using standardized untargeted gas chromatography-time-of-flight mass spectrometry (GC-TOFMS) metabolomics. Results: Metabolomics analyses of the BALF collected from the CysLTR1 KO mice presented significantly reduced levels of glucose, glucosamine, and glyceric acid, indicating the role of the CysLTR in lung glucose uptake and consequently lung glycolysis and gluconeogenesis. This is further supported by reductions in myo-inositol and D-chiro-inositol, also supporting previous findings that this occurs due to insulin resistance. Consequential disruption of various glucose-dependent pathways, including the pentose phosphate pathway (reduced gluconic acid, sedoheptulose and xylose) and purine metabolism (reduced 1-methylinosine) indicates a consequential altered nucleotide turnover, and the significantly reduced concentrations of butanoic acid, decan-2-ol, and 1-hexadecanol, indicate changes to fatty acid metabolism in the lung, as a compensatory response to the initial glucose deficiency induced by the CysLTR1 KO. Lastly, the changes to mandelic acid, glutaric acid, tricarballylic acid, and decan-2-ol, furthermore, indicate the role of CysLTR1 in the composition/metabolism of the microbiome. Conclusion: This study expands our knowledge on the role of CysLTR1 beyond its role in immune regulation, that may later serve towards a better understanding of CysLTR1 associated lung diseases and in the development of improved therapeutic strategies.
Indexed as
Identifiers
What OpenQuestion holds
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.