Evidence map›Paper›PMID 27939939›Full record

ReviewPharmacology & therapeutics2017

CD38 in the pathogenesis of allergic airway disease: Potential therapeutic targets.

Deepak A Deshpande, Alonso G P Guedes, Frances E Lund, Subbaya Subramanian, Timothy F Walseth, Mathur S Kannan

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Pharmacology & therapeutics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.1field-weighted citation impact, top 6% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 35 citations in OpenAlex.

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  4. The Role of NADBiomedicines · 2023
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 1 country.

Deepak A DeshpandeDepartment of Medicine, Thomas Jefferson University, Philadelphia, USA.
Alonso G P GuedesDepartment of Veterinary Clinical Sciences, University of Minnesota at Twin Cities, USA.
Frances E LundDepartment of Microbiology, University of Alabama at Birmingham, USA.
Subbaya SubramanianDepartment of Surgery, University of Minnesota at Twin Cities, USA.
Timothy F WalsethDepartment of Pharmacology, University of Minnesota at Twin Cities, USA.
Mathur S KannanDepartment of Veterinary and Biomedical Sciences, University of Minnesota at Twin Cities, USA. Electronic address: kanna001@umn.edu.
Twin Cities Orthopedics · USUniversity of Minnesota · USThomas Jefferson University · USUniversity of Alabama at Birmingham · US

Funding

MicroRNA regulation of CD38 and chemokine genes in human airway smooth muscleR21AI119395 · NIAID · UNIVERSITY OF MINNESOTA · PI KANNAN, MATHUR S · 2016 to 2017
$419k
NIAID NIH HHS R21 AI119395
6 · The paper itself

Abstract

CD38 is an ectoenzyme that catalyzes the conversion of β-nicotinamide adenine dinucleotide (β-NAD) to cyclic adenosine diphosphoribose (cADPR) and adenosine diphosphoribose (ADPR) and NADP to nicotinic acid adenine dinucleotide phosphate (NAADP) and adenosine diphosphoribose-2'-phosphate (ADPR-P). The metabolites of NAD and NADP have roles in calcium signaling in different cell types including airway smooth muscle (ASM) cells. In ASM cells, inflammatory cytokines augment CD38 expression and to a greater magnitude in cells from asthmatics, indicating a greater capacity for the generation of cADPR and ADPR in ASM from asthmatics. CD38 deficient mice develop attenuated airway responsiveness to inhaled methacholine following allergen sensitization and challenge compared to wild-type mice indicating its potential role in asthma. Regulation of CD38 expression in ASM cells is achieved by mitogen activated protein kinases, specific isoforms of PI3 kinases, the transcription factors NF-κB and AP-1, and post-transcriptionally by microRNAs. This review will focus on the role of CD38 in intracellular calcium regulation in ASM, contribution to airway inflammation and airway hyperresponsiveness in mouse models of allergic airway inflammation, the transcriptional and post-transcriptional mechanisms of regulation of expression, and outline approaches to inhibit its expression and activity.

Indexed as

ADP-ribosyl Cyclase 1AnimalsAsthmaCalciumCalcium SignalingDisease Models, AnimalGene Expression RegulationHumansInflammationMiceMicroRNAsMyocytes, Smooth MuscleNADNADPRespiratory HypersensitivityADP-ribosyl Cyclase 1CalciumMicroRNAsNADNADPAirway smooth muscleAsthmaCalcium regulationCD38MicroRNAs

Identifiers

PMID27939939
PMCPMC5346344
OpenAlexW2560056218

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.