Evidence map›Paper›PMID 25409170›Full record

ArticlePloS one2014

Pharmacological activation of the EDA/EDAR signaling pathway restores salivary gland function following radiation-induced damage.

Grace Hill, Denis Headon, Zoey I Harris, Kenneth Huttner, Kirsten H Limesand

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

18 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Cancer therapy-related salivary dysfunction.The Journal of clinical investigation · 2024
    Review
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  14. [Research progress in cell therapy and tissue engineering approach to regenerate salivary gland].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2017
    Review
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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

5 authors at 3 institutions in 2 countries.

Grace HillDepartment of Nutritional Sciences, University of Arizona, Tucson, Arizona, United States of America.
Denis HeadonThe Roslin Institute and Royal School of Veterinary Studies, University of Edinburgh, Edinburgh, United Kingdom.
Zoey I HarrisDepartment of Nutritional Sciences, University of Arizona, Tucson, Arizona, United States of America.
Kenneth HuttnerEdimer Pharmaceuticals Inc., Cambridge, Massachusetts, United States of America.
Kirsten H LimesandDepartment of Nutritional Sciences, University of Arizona, Tucson, Arizona, United States of America.
University of Arizona · USEdimer Pharmaceuticals (United States) · USRoslin Institute · GB

Funding

Mechanisms of IGF-1 mediated rescue of radiation-induced salivary gland dysfunctiR01DE018888 · NIDCR · UNIVERSITY OF ARIZONA · PI LIMESAND, KIRSTEN H · 2008 to 2012
$1.7M
NIDCR NIH HHS R01 DE018888NIDCR NIH HHS R01DE018888
6 · The paper itself

Abstract

Radiotherapy of head and neck cancers often results in collateral damage to adjacent salivary glands associated with clinically significant hyposalivation and xerostomia. Due to the reduced capacity of salivary glands to regenerate, hyposalivation is treated by substitution with artificial saliva, rather than through functional restoration of the glands. During embryogenesis, the ectodysplasin/ectodysplasin receptor (EDA/EDAR) signaling pathway is a critical element in the development and growth of salivary glands. We have assessed the effects of pharmacological activation of this pathway in a mouse model of radiation-induced salivary gland dysfunction. We report that post-irradiation administration of an EDAR-agonist monoclonal antibody (mAbEDAR1) normalizes function of radiation damaged adult salivary glands as determined by stimulated salivary flow rates. In addition, salivary gland structure and homeostasis is restored to pre-irradiation levels. These results suggest that transient activation of pathways involved in salivary gland development could facilitate regeneration and restoration of function following damage.

Indexed as

AmylasesAnimalsAntibodies, MonoclonalCell ProliferationEctodysplasinsEdar ReceptorFemaleHead and Neck NeoplasmsMiceRecovery of FunctionSalivaSalivary GlandsSignal TransductionTime FactorsVacuolesAmylasesAntibodies, MonoclonalEctodysplasinsEda protein, mouseEdar protein, mouseEdar Receptor

Identifiers

PMID25409170
PMCPMC4237357
OpenAlexW2092348552

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.