ArticleBritish journal of pharmacology2020
Functional contribution of sphingosine-1-phosphate to airway pathology in cigarette smoke-exposed mice.
Article in British journal of pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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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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
16 citing papers in PubMed, 19 citations in OpenAlex.
- Increasing S1P promotes M1 macrophage in chronic obstructive pulmonary disease and chronic obstructive pulmonary disease-obstructive sleep apnea overlap syndrome via S1PR1/HDAC1 signaling.Journal of thoracic disease · 2025Article
- Serum metabolomics analysis of patients with chronic obstructive pulmonary disease and 'frequent exacerbator' phenotype.Molecular medicine reports · 2024Article
- New Therapeutic Options in Pulmonal Diseases: Sphingolipids and Modulation of Sphingolipid Metabolism.Handbook of experimental pharmacology · 2024Review
- Immunohistochemical Study of Airways Fibrous Remodeling in Smoking Mice.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2023Article
- The Ying and Yang of Sphingosine-1-Phosphate Signalling within the Bone.International journal of molecular sciences · 2023Review
- Deletion of sphingosine kinase 2 attenuates cigarette smoke-mediated chronic obstructive pulmonary disease-like symptoms by reducing lung inflammation.Biomolecules & biomedicine · 2023Article
- Lung microRNAs Expression in Lung Cancer and COPD: A Preliminary Study.Biomedicines · 2023Article
- The effects of epithelial-mesenchymal transitions in COPD induced by cigarette smoke: an update.Respiratory research · 2022Review
- Smoking Cessation in Mice Does Not Switch off Persistent Lung Inflammation and Does Not Restore the Expression of HDAC2 and SIRT1.International journal of molecular sciences · 2022Article
- Sphingosine-1-phosphate/TGF-β axis drives epithelial mesenchymal transition in asthma-like disease.British journal of pharmacology · 2022Article
- Associations among S100A4, Sphingosine-1-Phosphate, and Pulmonary Function in Patients with Chronic Obstructive Pulmonary Disease.Oxidative medicine and cellular longevity · 2022Article
- Lysophospholipids in Lung Inflammatory Diseases.Advances in experimental medicine and biology · 2021Article
- Iron and Sphingolipids as Common Players of (Mal)Adaptation to Hypoxia in Pulmonary Diseases.International journal of molecular sciences · 2020Review
- Functional contribution of sphingosine-1-phosphate to airway pathology in cigarette smoke-exposed mice.British journal of pharmacology · 2020Article
- Innate Immunity and Cell Surface Receptors in the Pathogenesis of COPD: Insights from Mouse Smoking Models.International journal of chronic obstructive pulmonary disease · 2020Review
- Breakthroughs in Medicinal Chemistry: New Targets and Mechanisms, New Drugs, New Hopes-6.Molecules (Basel, Switzerland) · 2019Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
Abstract
background and purposeA critical role for sphingosine kinase/sphingosine-1-phosphate (S1P) pathway in the control of airway function has been demonstrated in respiratory diseases. Here, we address S1P contribution in a mouse model of mild chronic obstructive pulmonary disease (COPD). EXPERIMENTAL APPROACH: C57BL/6J mice have been exposed to room air or cigarette smoke up to 11 months and killed at different time points. Functional and molecular studies have been performed. KEY
resultsCigarette smoke caused emphysematous changes throughout the lung parenchyma coupled to a progressive collagen deposition in both peribronchiolar and peribronchial areas. The high and low airways showed an increased reactivity to cholinergic stimulation and α-smooth muscle actin overexpression. Similarly, an increase in airway reactivity and lung resistances following S1P challenge occurred in smoking mice. A high expression of S1P, Sph-K CONCLUSIONS AND IMPLICATIONS: S1P signalling up-regulation follows the disease progression in smoking mice and is involved in the development of airway hyperresponsiveness. Our study defines a therapeutic potential for S1P inhibitors in management of airways hyperresponsiveness associated to emphysema in smokers with both asthma and COPD.
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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.