Evidence map›Paper›PMID 33419308›Full record

ArticleCells2020

Implication of the Association of Fibrinogen Citrullination and Osteoclastogenesis in Bone Destruction in Rheumatoid Arthritis.

Ji Soo Kim, Mikyung Choi, Ji Yong Choi, Joo Yeon Kim, Jeong Yeon Kim, Jin-Su Song, Lionel B Ivashkiv, Eun Young Lee

Open access · goldAbstract read
In one paragraph

Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

32 citing papers in PubMed, 38 citations in OpenAlex.

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  11. Investigating the Potential of CDDO-Me as an HMGB1 Inhibitor in Mitigating Cerebral Ischemia-Reperfusion Injury.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 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

8 authors at 2 institutions in 2 countries.

Ji Soo KimDepartment of Family Medicine, Seoul National University Hospital, Seoul 03080, Korea.
Mikyung ChoiDepartment of Chemistry, Seoul National University, Seoul 08826, Korea.
Ji Yong ChoiDivision of Rheumatology, Department of Internal Medicine, Seoul National University College of Medicine, Seoul 03080, Korea.
Joo Yeon KimDivision of Rheumatology, Department of Internal Medicine, Seoul National University College of Medicine, Seoul 03080, Korea.
Jeong Yeon KimDivision of Rheumatology, Department of Internal Medicine, Seoul National University College of Medicine, Seoul 03080, Korea.
Jin-Su SongDepartment of Chemistry, Seoul National University, Seoul 08826, Korea.
Lionel B IvashkivArthritis and Tissue Degeneration Program and David C. Rosensweig Center for Genomics Research, Hospital for Special Surgery, New York, NY 10021, USA.
Eun Young LeeDivision of Rheumatology, Department of Internal Medicine, Seoul National University College of Medicine, Seoul 03080, Korea.ORCID 0000-0001-6975-8627
Seoul National University · KRHospital for Special Surgery · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immune complexes containing citrullinated fibrinogen are present in the sera and synovium of rheumatoid arthritis patients and potentially contribute to synovitis. However, fibrinogen can inhibit the osteoclastogenesis of precursor cells. We investigated the direct effect of citrullinated fibrinogen on osteoclastogenesis to understand the role of citrullination on bone erosion of rheumatoid arthritis patients. We evaluated the fibrinogen citrullination sites using mass spectrometry and quantified osteoclast-related protein and gene expression levels by Western blotting, microarray, and real-time polymerase chain reaction. Differences in spectral peaks were noted between fibrinogen and citrullinated fibrinogen at five sites in α-chains, two sites in β-chains, and one site in a γ-chain. Transcriptome changes induced by fibrinogen and citrullinated fibrinogen were identified and differentially expressed genes grouped into three distinctive modules. Fibrinogen was then citrullinated in vitro using peptidylarginine deiminase. When increasing doses of soluble fibrinogen and citrullinated fibrinogen were applied to human CD14+ monocytes, citrullination restored osteoclastogenesis-associated changes, including NF-ATc1 and ß3-integrin. Finally, citrullination rescued the number of osteoclasts by restoring fibrinogen-induced suppression of osteoclastogenesis. Taken together, the results indicate that the inhibitory function of fibrinogen on osteoclastogenesis is reversed by citrullination and suggest that citrullinated fibrinogen may contribute to erosive bone destruction in rheumatoid arthritis.

Indexed as

CitrullinationOsteogenesisAnimalsArthritis, RheumatoidBone and BonesBone ResorptionCattleCell DifferentiationCitrullineFibrinogenHumansInflammationIntegrin beta3Leukocytes, MononuclearLipopolysaccharide ReceptorsNFATC Transcription FactorsCD14 protein, humanCitrullineFibrinogenIntegrin beta3Lipopolysaccharide ReceptorsNFATC Transcription Factorscitrullinated fibrinogenosteoclastogenesisrheumatoid arthritis

Identifiers

PMID33419308
PMCPMC7766778
OpenAlexW3114437182

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.