Evidence map›Paper›PMID 27860453›Full record

ArticleArthritis & rheumatology (Hoboken, N.J.)2017

Targeting the D Series Resolvin Receptor System for the Treatment of Osteoarthritis Pain.

Junting Huang, James J Burston, Li Li, Sadaf Ashraf, Paul I Mapp, Andrew J Bennett, Srinivasarao Ravipati, Petros Pousinis, David A Barrett, Brigitte E Scammell and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Arthritis & rheumatology (Hoboken, N.J.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 7% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

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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

11 authors at 1 institution in 1 country.

Junting HuangUniversity of Nottingham, Nottingham, UK.
James J BurstonUniversity of Nottingham, Nottingham, UK.
Li LiUniversity of Nottingham, Nottingham, UK.
Sadaf AshrafUniversity of Nottingham, Nottingham, UK.
Paul I MappUniversity of Nottingham, Nottingham, UK.
Andrew J BennettUniversity of Nottingham, Nottingham, UK.
Srinivasarao RavipatiUniversity of Nottingham, Nottingham, UK.
Petros PousinisUniversity of Nottingham, Nottingham, UK.
David A BarrettUniversity of Nottingham, Nottingham, UK.
Brigitte E ScammellUniversity of Nottingham, Nottingham, UK.
Victoria ChapmanUniversity of Nottingham, Nottingham, UK.
University of Nottingham · GB

Funding

Arthritis Research UK 18769
6 · The paper itself

Abstract

objectivePain is a major symptom of osteoarthritis (OA); currently available analgesics either do not provide adequate pain relief or are associated with serious side effects. The aim of this study was to investigate the therapeutic potential of targeting the resolvin receptor system to modify OA pain and pathology.

methodsGene expression of 2 resolvin receptors (ALX and ChemR23) was quantified in synovium and medial tibial plateau specimens obtained from patients with OA at the time of joint replacement surgery. Two models of OA joint pain were used for the mechanistic studies. Gene expression in the joint and central nervous system was quantified. The effects of exogenous administration of the D series resolvin precursor 17(R)-hydroxy-docosahexaenoic acid (17[R]-HDoHE) on pain behavior, joint pathology, spinal microglia, and astroglyosis were quantified. Plasma levels of relevant lipids, resolvin D2, 17(R)-HDoHE, and arachidonic acid, were determined in rats, using liquid chromatography tandem mass spectrometry.

resultsThere was a positive correlation between resolvin receptor and interleukin-6 (IL-6) expression in human OA synovial and medial tibial plateau tissue. In rats, synovial expression of ALX was positively correlated with expression of IL-1β, tumor necrosis factor, and cyclooxygenase 2. Treatment with 17(R)-HDoHE reversed established pain behavior (but not joint pathology) in 2 models of OA pain. This was associated with a significant elevation in the plasma levels of resolvin D2 and a significant reduction in astrogliosis in the spinal cord in the monosodium iodoacetate-induced OA rat model.

conclusionOur preclinical data demonstrate the robust analgesic effects of activation of the D series resolvin pathways in 2 different animal models of OA. Our data support a predominant central mechanism of action in clinically relevant models of OA pain.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsArthralgiaBehavior, AnimalCartilage, ArticularDisease Models, AnimalDocosahexaenoic AcidsEnzyme InhibitorsGene ExpressionHumansIodoacetic AcidMenisci, TibialNeurogliaOsteoarthritis, KneeRatsReal-Time Polymerase Chain Reaction17-hydroxy-4,7,10,13,15,19-docosahexaenoic acidAdaptor Proteins, Signal TransducingCMKLR1 protein, humanCmklr1 protein, ratDocosahexaenoic AcidsEnzyme InhibitorsHSH2D protein, humanIodoacetic Acidlipoxin A(4) receptor, ratReceptors, ChemokineReceptors, LipoxinRNA, Messenger

Identifiers

PMID27860453
PMCPMC5763389
OpenAlexW2552234711

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Registered trials

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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.