Evidence map›Paper›PMID 22634112›Full record

ReviewPulmonary pharmacology & therapeutics2013

cAMP regulation of airway smooth muscle function.

Charlotte K Billington, Oluwaseun O Ojo, Raymond B Penn, Satoru Ito

Abstract readReview
In one paragraph

Review in Pulmonary pharmacology & therapeutics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed, 1 pooled it
8.4field-weighted citation impact, top 2% 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

110 citing papers in PubMed, 1 synthesis or guideline pooled it, 237 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
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  18. Article
  19. GOA-1 regulates spermathecal transits.microPublication biology · 2025
    Article
  20. Article

50 more citing papers are in PubMed but not listed here.

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

4 authors at 4 institutions in 4 countries.

Charlotte K BillingtonDivision of Therapeutics and Molecular Medicine, The University of Nottingham, Nottingham NG7 2UH, UK. charlotte.billington@nottingham.ac.uk
Oluwaseun O Ojo
Raymond B Penn
Satoru Ito
Nagoya University · JPUniversity of Manitoba · CAUniversity of Maryland, Baltimore · USUniversity of Nottingham · GB

Funding

G Protein-Coupled Receptor Signaling in Airway Smooth MuR01HL058506 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI RAYMOND B. PENN · 2001 to 2026
$9.3M
Arrestin Selectivity for GPCRs in Airway Smooth MuscleR01HL093103 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI PENN, RAYMOND B., WALKER, JULIA K L · 2010 to 2013
$1.5M
OGR1 is a proton-sensing GPCR in airway smooth muscleR21HL108071 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI PENN, RAYMOND B. · 2011 to 2012
$453k
BETA ADRENERGIC RECEPTOR REGULATION IN HUMAN AIRWAY MUSCR29HL058506 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI PENN, RAYMOND B. · 1997 to 2000
$113k
CIHRMedical Research Council G0400910Medical Research Council G0701390Medical Research Council G1000861NHLBI NIH HHS HL093103NHLBI NIH HHS HL108071NHLBI NIH HHS HL58506NHLBI NIH HHS R01 HL058506NHLBI NIH HHS R01 HL093103NHLBI NIH HHS R21 HL108071NHLBI NIH HHS R29 HL058506
6 · The paper itself

Abstract

Agonists activating β(2)-adrenoceptors (β(2)ARs) on airway smooth muscle (ASM) are the drug of choice for rescue from acute bronchoconstriction in patients with both asthma and chronic obstructive pulmonary disease (COPD). Moreover, the use of long-acting β-agonists combined with inhaled corticosteroids constitutes an important maintenance therapy for these diseases. β-Agonists are effective bronchodilators due primarily to their ability to antagonize ASM contraction. The presumed cellular mechanism of action involves the generation of intracellular cAMP, which in turn can activate the effector molecules cAMP-dependent protein kinase (PKA) and Epac. Other agents such as prostaglandin E(2) and phosphodiesterase inhibitors that also increase intracellular cAMP levels in ASM, can also antagonize ASM contraction, and inhibit other ASM functions including proliferation and migration. Therefore, β(2)ARs and cAMP are key players in combating the pathophysiology of airway narrowing and remodeling. However, limitations of β-agonist therapy due to drug tachyphylaxis related to β(2)AR desensitization, and recent findings regarding the manner in which β(2)ARs and cAMP signal, have raised new and interesting questions about these well-studied molecules. In this review we discuss current concepts regarding β(2)ARs and cAMP in the regulation of ASM cell functions and their therapeutic roles in asthma and COPD.

Indexed as

Adrenergic beta-2 Receptor AgonistsAnimalsAsthmaBronchoconstrictionCyclic AMPDrug Therapy, CombinationGlucocorticoidsHumansMuscle, SmoothPulmonary Disease, Chronic ObstructiveReceptors, Adrenergic, beta-2Adrenergic beta-2 Receptor AgonistsCyclic AMPGlucocorticoidsReceptors, Adrenergic, beta-2

Identifiers

PMID22634112
PMCPMC3574867
OpenAlexW2057946435

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.