Evidence map›Paper›PMID 28298636›Full record

ArticleScientific reports2017

The purinergic receptor P2X5 regulates inflammasome activity and hyper-multinucleation of murine osteoclasts.

Hyunsoo Kim, Matthew C Walsh, Noriko Takegahara, Sarah A Middleton, Hong-In Shin, Junhyong Kim, Yongwon Choi

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 5% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

  1. Pooled it
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  5. Possible Roles for Purinergic Receptor P2RX4 in Breast and Prostate Cancers.International journal of molecular sciences · 2025
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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

7 authors at 2 institutions in 3 countries.

Hyunsoo KimDepartment of Pathology and Laboratory Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, 19104, USA.
Matthew C WalshDepartment of Pathology and Laboratory Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, 19104, USA.
Noriko TakegaharaDepartment of Pathology and Laboratory Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, 19104, USA.
Sarah A MiddletonDepartment of Biology, Department of Computer and Information Science, School of Arts and Sciences, Program in Single Cell Biology, University of Pennsylvania, Philadelphia, PA, 19104, USA.ORCID 0000-0002-9504-2574
Hong-In ShinIHBR, Department of Oral Pathology, School of Dentistry, Kyungpook National University, Daegu, 700412, South Korea.
Junhyong KimDepartment of Biology, Department of Computer and Information Science, School of Arts and Sciences, Program in Single Cell Biology, University of Pennsylvania, Philadelphia, PA, 19104, USA.
Yongwon ChoiDepartment of Pathology and Laboratory Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, 19104, USA. ychoi3@mail.med.upenn.edu.
University of Pennsylvania · USKyungpook National University · KR

Funding

Molecular regulation of osteoclast maturationR01AR067726 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI CHOI, YONGWON · 2015 to 2018
$1.4M
NIAMS NIH HHS R01 AR067726
6 · The paper itself

Abstract

Excessive bone resorption by osteoclasts (OCs) can result in serious clinical outcomes, including bone loss that may weaken skeletal or periodontal strength. Proper bone homeostasis and skeletal strength are maintained by balancing OC function with the bone-forming function of osteoblasts. Unfortunately, current treatments that broadly inhibit OC differentiation or function may also interfere with coupled bone formation. We therefore identified a factor, the purinergic receptor P2X5 that is highly expressed during the OC maturation phase, and which we show here plays no apparent role in early bone development and homeostasis, but which is required for osteoclast-mediated inflammatory bone loss and hyper-multinucleation of OCs. We further demonstrate that P2X5 is required for ATP-mediated inflammasome activation and IL-1β production by OCs, and that P2X5-deficient OC maturation is rescued in vitro by addition of exogenous IL-1β. These findings identify a mechanism by which OCs react to inflammatory stimuli, and may identify purinergic signaling as a therapeutic target for bone loss-related inflammatory conditions.

Indexed as

Adenosine TriphosphateAnimalsBone DevelopmentCell DifferentiationCells, CulturedGene Knockdown TechniquesHumansInflammasomesInterleukin-1betaLipopolysaccharidesMiceOsteoclastsPolymorphism, Single NucleotideReceptors, Purinergic P2X5Adenosine TriphosphateIL1B protein, mouseInflammasomesInterleukin-1betaLipopolysaccharidesP2rx5 protein, mouseReceptors, Purinergic P2X5

Identifiers

PMID28298636
PMCPMC5427844
OpenAlexW2593185740

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.