Evidence map›Paper›PMID 30915215›Full record

ArticleBone & joint research2019

NFAT1 protects articular cartilage against osteoarthritic degradation by directly regulating transcription of specific anabolic and catabolic genes.

M Zhang, Q Lu, T Budden, J Wang

Open access · goldAbstract read
In one paragraph

Article in Bone & joint research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

9 citing papers in PubMed, 17 citations in OpenAlex.

  1. Biomedicines · 2025
    Review
  2. Article
  3. Intergenic Interactions ofLife (Basel, Switzerland) · 2023
    Article
  4. Regulatory role of NFAT1 signaling in articular chondrocyte activities and osteoarthritis pathogenesis.Biocell : official journal of the Sociedades Latinoamericanas de Microscopia Electronica ... et. al · 2023
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Regulatory mechanisms and clinical manifestations of musculoskeletal aging.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2019
    Review
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

4 authors at 1 institution in 1 country.

M ZhangHarrington Laboratory for Molecular Orthopedics, Department of Orthopedic Surgery; The Division of Allergy, Clinical Immunology and Rheumatology, Department of Medicine, University of Kansas Medical Center, Kansas City, Kansas, USA.
Q LuHarrington Laboratory for Molecular Orthopedics, Department of Orthopedic Surgery, University of KansasMedical Center, Kansas City, Kansas, USA.
T BuddenHarrington Laboratory for Molecular Orthopedics, Department of Orthopedic Surgery, University of KansasMedical Center, Kansas City, Kansas, USA.
J WangHarrington Laboratory for Molecular Orthopedics, Department of Orthopedic Surgery; and Department of Biochemistry & Molecular Biology, University of Kansas Medical Center, Kansas City, Kansas, USA.
University of Kansas Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesAdult mice lacking the transcription factor NFAT1 exhibit osteoarthritis (OA). The precise molecular mechanism for NFAT1 deficiency-induced osteoarthritic cartilage degradation remains to be clarified. This study aimed to investigate if NFAT1 protects articular cartilage (AC) against OA by directly regulating the transcription of specific catabolic and anabolic genes in articular chondrocytes.

methodsThrough a combined approach of gene expression analysis and web-based searching of NFAT1 binding sequences, 25 candidate target genes that displayed aberrant expression in

resultsChromatin immunoprecipitation assays revealed that NFAT1 bound directly to the promoter of 21 of the 25 tested genes encoding cartilage-matrix proteins, growth factors, inflammatory cytokines, matrix-degrading proteinases, and specific transcription factors. Promoter luciferase reporter assays of representative anabolic and catabolic genes demonstrated that NFAT1-DNA binding functionally regulated the luciferase activity of specific target genes in wild-type chondrocytes, but not in

conclusionNFAT1 protects AC against degradation by directly regulating the transcription of target genes in articular chondrocytes. NFAT1 deficiency causes defective transcription of specific anabolic and catabolic genes in articular chondrocytes, leading to increased matrix catabolism and osteoarthritic cartilage degradation.

Indexed as

Chromatin immunoprecipitationGene expressionNFAT1OsteoarthritisPromoter luciferase reporter assay

Identifiers

PMID30915215
PMCPMC6397328
OpenAlexW2918222004

What OpenQuestion holds

Textmetadata
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.