Evidence map›Paper›PMID 25575966›Full record

ArticleOsteoarthritis and cartilage2015

Insights into osteoarthritis progression revealed by analyses of both knee tibiofemoral compartments.

C-H Chou, M T M Lee, I-W Song, L-S Lu, H-C Shen, C-H Lee, J-Y Wu, Y-T Chen, V B Kraus, C-C Wu

Abstract readComparative Study
In one paragraph

Article in Osteoarthritis and cartilage, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 9% 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

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

  1. Pooled it
  2. CSPG4Osteoarthritis and cartilage open · 2026
    Article
  3. The role of IL-11 in chronic diseases.Frontiers in immunology · 2026
    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

10 authors at 5 institutions in 3 countries.

C-H ChouInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan; National Center for Genome Medicine, Academia Sinica, Taipei, Taiwan; Department of Pathology, Duke University School of Medicine, Durham, NC, USA. Electronic address: cc380@duke.edu.
M T M LeeInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan; National Center for Genome Medicine, Academia Sinica, Taipei, Taiwan; Graduate Institute of Chinese Medical Science, China Medical University, Taichung, Taiwan; Laboratory for International Alliance, RIKEN Center for Genomic Medicine, Yokohama, Japan. Electronic address: mikelee@src.riken.jp.
I-W SongInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan; National Center for Genome Medicine, Academia Sinica, Taipei, Taiwan; Graduate Institute of Life Sciences, National Defense Medical Center, Taipei, Taiwan. Electronic address: iwsong16@yahoo.com.tw.
L-S LuInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan; National Center for Genome Medicine, Academia Sinica, Taipei, Taiwan. Electronic address: liangsuei@gmail.com.
H-C ShenDepartment of Orthopaedic Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan. Electronic address: doc20231@gmail.com.
C-H LeeDepartment of Orthopedics, School of Medicine, College of Medicine, Taipei Medical University, Taiwan; Department of Orthopedics, Taipei Medical University Hospital, Taiwan. Electronic address: chianherlee@yahoo.com.tw.
J-Y WuInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan; National Center for Genome Medicine, Academia Sinica, Taipei, Taiwan; Translational Resource Center for Genomic Medicine, Academia Sinica, Taipei, Taiwan. Electronic address: jywu@ibms.sinica.edu.tw.
Y-T ChenInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan; Department of Pediatrics, Duke University School of Medicine, Durham, NC, USA. Electronic address: chen0010@ibms.sinica.edu.tw.
V B KrausDuke Molecular Physiology Institute, Department of Medicine, Duke University School of Medicine, Durham, NC, USA; Department of Pathology, Duke University School of Medicine, Durham, NC, USA. Electronic address: vbk@duke.edu.
C-C WuDepartment of Orthopaedic Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan. Electronic address: doc20281@gmail.com.
Duke University · USGenomics Research Center, Academia Sinica · TWTri-Service General Hospital · TWChina Medical University · TWTaipei Medical University Hospital · TW

Funding

Resource Core 3 - Metabolomics CoreP30AG028716 · NIA · DUKE UNIVERSITY · PI CATHLEEN S COLON-EMERIC, Susan Nicole Hastings · 2006 to 2026
$24.6M
Thermally-Triggered Intra-articular Drug Delivery for OAP01AR050245 · NIAMS · DUKE UNIVERSITY · PI GUILAK, FARSHID · 2003 to 2012
$11.5M
NIAMS NIH HHS P01 AR050245NIAMS NIH HHS P01 AR50245NIA NIH HHS 5P30 AG028716NIA NIH HHS P30 AG028716
6 · The paper itself

Abstract

objectiveTo identify disease relevant genes and pathways associated with knee Osteoarthritis (OA) progression in human subjects using medial and lateral compartment dominant OA knee tissue.

designGene expression of knee cartilage was comprehensively assessed for three regions of interest from human medial dominant OA (n = 10) and non-OA (n = 6) specimens. Histology and gene expression were compared for the regions with minimal degeneration, moderate degeneration and significant degeneration. Agilent whole-genome microarray was performed and data were analyzed using Agilent GeneSpring GX11.5. Significant differentially regulated genes were further investigated by Ingenuity Pathway Analysis (IPA) to identify functional categories. To confirm their association with disease severity as opposed to site within the knee, 30 differentially expressed genes, identified by microarray, were analyzed by quantitative reverse-transcription polymerase chain reaction on additional medial (n = 16) and lateral (n = 10) compartment dominant knee OA samples.

resultsA total of 767 genes were differentially expressed ≥ two-fold (P ≤ 0.05) in lesion compared to relatively intact regions. Analysis of these data by IPA predicted biological functions related to an imbalance of anabolism and catabolism of cartilage matrix components. Up-regulated expression of IL11, POSTN, TNFAIP6, and down-regulated expression of CHRDL2, MATN4, SPOCK3, VIT, PDE3B were significantly associated with OA progression and validated in both medial and lateral compartment dominant OA samples.

conclusionsOur study provides a strategy for identifying targets whose modification may have the potential to ameliorate pathological alternations and progression of disease in cartilage and to serve as biomarkers for identifying individuals susceptible to progression.

Indexed as

Disease ProgressionAgedAged, 80 and overBiomechanical PhenomenaCartilage, ArticularFemaleFemurHumansKnee JointMaleMicroarray AnalysisMiddle AgedOsteoarthritis, KneeSeverity of Illness IndexTibiaTranscriptomeCartilageLateral knee compartmentMicroarrayOsteoarthritis progression

Identifiers

PMID25575966
PMCPMC4814163
OpenAlexW2078149335

What Socratic 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 Socratic graph.