ReviewCanadian journal of physiology and pharmacology2015
CD38 and airway hyper-responsiveness: studies on human airway smooth muscle cells and mouse models.
Review in Canadian journal of physiology and pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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
23 citing papers in PubMed, 42 citations in OpenAlex.
- PFKM acts as a metabolic switch initiating donut-shaped mitochondrial remodeling to promote osteogenesis.International journal of oral science · 2026Article
- Retention of stress susceptibility in the mdx mouse model of Duchenne muscular dystrophy after PGC-1α overexpression or ablation of IDO1 or CD38.Human molecular genetics · 2024Article
- Mechanistic Links Between Obesity and Airway Pathobiology Inform Therapies for Obesity-Related Asthma.Paediatric drugs · 2023Review
- Eliminating the monitoring period with subcutaneous daratumumab: a single-center experience.Blood cancer journal · 2023Article
- Review
- Review
- CD38-NADase is a new major contributor to Duchenne muscular dystrophic phenotype.EMBO molecular medicine · 2022Article
- Daratumumab monotherapy in relapsed and refractory multiple myeloma patients with severely compromised forced expiratory volume in one second.Blood research · 2022Article
- Nicotinic α7 acetylcholine receptor (α7nAChR) in human airway smooth muscle.Archives of biochemistry and biophysics · 2021Article
- CD38 deficiency alleviates Ang II-induced vascular remodeling by inhibiting small extracellular vesicle-mediated vascular smooth muscle cell senescence in mice.Signal transduction and targeted therapy · 2021Article
- Downregulation of miR-140-3p Contributes to Upregulation of CD38 Protein in Bronchial Smooth Muscle Cells.International journal of molecular sciences · 2020Article
- Novel Pathway of Adenosine Generation in the Lungs from NADMolecules (Basel, Switzerland) · 2020Article
- Article
- Bisphenol A Activates an Innate Viral Immune Response Pathway.Journal of proteome research · 2020Article
- Evaluation of cationic channel TRPV2 as a novel biomarker and therapeutic target in Leukemia-Implications concerning the resolution of pulmonary inflammation.Scientific reports · 2019Article
- Protective Role of Autophagy in Nlrp3 Inflammasome Activation and Medial Thickening of Mouse Coronary Arteries.The American journal of pathology · 2018Article
- CD38 in the pathogenesis of allergic airway disease: Potential therapeutic targets.Pharmacology & therapeutics · 2017Review
- Emerging concepts in smooth muscle contributions to airway structure and function: implications for health and disease.American journal of physiology. Lung cellular and molecular physiology · 2016Review
- Mechanisms of BDNF regulation in asthmatic airway smooth muscle.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Blocking Cyclic Adenosine Diphosphate Ribose-mediated Calcium Overload Attenuates Sepsis-induced Acute Lung Injury in Rats.Chinese medical journal · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 5 institutions in 1 country.
Funding
Abstract
Asthma is an inflammatory disease in which altered calcium regulation, contractility, and airway smooth muscle (ASM) proliferation contribute to airway hyper-responsiveness and airway wall remodeling. The enzymatic activity of CD38, a cell-surface protein expressed in human ASM cells, generates calcium mobilizing second messenger molecules such as cyclic ADP-ribose. CD38 expression in human ASM cells is augmented by cytokines (e.g., TNF-α) that requires the activation of MAP kinases and the transcription factors, NF-κB and AP-1, and is post-transcriptionally regulated by miR-140-3p and miR-708 by binding to 3' Untranslated Region of CD38 as well as by modulating the activation of signaling mechanisms involved in its regulation. Mice deficient in Cd38 exhibit reduced airway responsiveness to inhaled methacholine relative to the response in wild-type mice. Intranasal challenge of Cd38-deficient mice with TNF-α or IL-13, or the environmental fungus Alternaria alternata, causes significantly attenuated methacholine responsiveness compared with wild-type mice, with comparable airway inflammation. Reciprocal bone marrow transfer studies revealed partial restoration of airway hyper-responsiveness to inhaled methacholine in the Cd38-deficient mice. These studies provide evidence for CD38 involvement in the development of airway hyper-responsiveness; a hallmark feature of asthma. Future studies aimed at drug discovery and delivery targeting CD38 expression and (or) activity are warranted.
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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.