Evidence map›Paper›PMID 26707989›Full record

ReviewOsteoarthritis and cartilage2016

Osteoarthritis year in review 2015: biology.

A M Malfait

Open access · bronzeAbstract readReview
In one paragraph

Review in Osteoarthritis and cartilage, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 1 pooled it
14.2field-weighted citation impact, top 1% 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

74 citing papers in PubMed, 1 synthesis or guideline pooled it, 161 citations in OpenAlex.

  1. Pooled it
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  13. KLF transcription factors in bone diseases.Journal of cellular and molecular medicine · 2024
    Review
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14 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

1 author at 1 institution in 1 country.

A M MalfaitDepartment of Internal Medicine, Division of Rheumatology, Rush University Medical Center, Chicago, IL, USA; Department of Biochemistry, Rush University Medical Center, Chicago, IL, USA. Electronic address: annemarie@annemariemalfait.com.
Rush University Medical Center · US

Funding

Osteoarthritis Progression And Sensory Pathway AlterationsR01AR064251 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI MALFAIT, ANNE-MARIE, MILLER, RICHARD J · 2013 to 2025
$7.6M
Molecular Pathways of Pain Generation in OsteoarthritisR01AR060364 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI MALFAIT, ANNE-MARIE · 2011 to 2025
$6.0M
NIAMS NIH HHS R01 AR060364NIAMS NIH HHS R01AR060364NIAMS NIH HHS R01 AR064251NIAMS NIH HHS R01AR064251
6 · The paper itself

Abstract

This review highlights a selection of recently published literature in the area of osteoarthritis biology. Major themes transpiring from a PubMed search covering the year between the 2014 and the 2015 Osteoarthritis Research Society International (OARSI) World Congress are explored. Inflammation emerged as a significant theme, revealing complex pathways that drive dramatic changes in cartilage homeostasis and in the synovium. Highlights include a homeostatic role for CXC chemokines in cartilage, identification of the zinc-ZIP8-MTF1 axis as an essential regulator of cartilage catabolism, and the discovery that a small aggrecan fragment can have catabolic and pro-inflammatory effects through Toll-like receptor 2. Synovitis can promote joint damage, partly through alarmins such as S100A8. Synovitis and synovial expression of the pro-algesic neurotrophin, Nerve Growth Factor, are associated with pain. Increasingly, researchers are considering specific pathogenic pathways that may operate in distinct subsets of osteoarthritis associated with distinct risk factors, including obesity, age, and joint injury. In obesity, the contribution of metabolic factors and diet is under intense investigation. The role of autophagy and oxidative stress in age-related osteoarthritis has been further explored. This approach may open avenues for targeted treatment of distinct phenotypes of osteoarthritis. Finally, a small selection of novel analgesic targets in the periphery is briefly discussed, including calcitonin gene-related peptide and the neuronal sodium voltage-gated channels, Nav1.7 and Nav1.8.

Indexed as

AutophagyCalcitonin Gene-Related PeptideCalgranulin ACartilage, ArticularCation Transport ProteinsChemokines, CXCDNA-Binding ProteinsHumansInflammationNAV1.7 Voltage-Gated Sodium ChannelNAV1.8 Voltage-Gated Sodium ChannelNerve Growth FactorObesityOsteoarthritisOxidative StressSynovial MembraneCalcitonin Gene-Related PeptideCalgranulin ACation Transport ProteinsChemokines, CXCDNA-Binding ProteinsNAV1.7 Voltage-Gated Sodium ChannelNAV1.8 Voltage-Gated Sodium ChannelNerve Growth FactorSCN10A protein, humanSCN9A protein, humanSLC39A8 protein, humanTLR2 protein, humanToll-Like Receptor 2Transcription Factor MTF-1Transcription FactorsZincCartilageChondrocytesInflammationOsteoarthritisPainSynovium

Identifiers

PMID26707989
PMCPMC4693144
OpenAlexW2208583540

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.