Evidence map›Paper›PMID 36253500›Full record

ArticleInflammation2023

Dimethyl Fumarate Inhibits Fibroblast Like Synoviocytes-mediated Inflammation and Joint Destruction in Rheumatoid Arthritis.

Parisa Zafari, Mahdi Taghadosi, Fatemeh Faramarzi, Misagh Rajabinejad, Alireza Rafiei

Abstract read
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In one paragraph

Article in Inflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
3.2field-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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. Pooled it
  2. Review
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  6. Review
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  10. The stimulator of interferon genes (STING) agonists for treating acute myeloid leukemia (AML): current knowledge and future outlook.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    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

5 authors at 2 institutions in 1 country.

Parisa ZafariDepartment of Immunology, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran.
Mahdi TaghadosiDepartment of Immunology, Faculty of Medicine, Kermanshah University of Medical Sciences, Kermanshah, Iran.
Fatemeh FaramarziDepartment of Immunology, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran.
Misagh RajabinejadDepartment of Immunology, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran.
Alireza RafieiDepartment of Immunology, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran. rafiei1710@gmail.com.ORCID http://orcid.org/0000-0002-1766-6605
Mazandaran University of Medical Sciences · IRKermanshah University of Medical Sciences · IR

Funding

Mazandaran University of Medical Sciences 3123
6 · The paper itself

Abstract

Rheumatoid arthritis (RA) as a chronic inflammatory disorder affects around 1% of the world population. Fibroblast-like synoviocyte (FLS), one of the main cells in RA pathogenesis is characterized by hyperproliferation and resistance to apoptosis resulting to synovial hyperplasia. Dimethyl fumarate (DMF) has been licensed for the treatment of multiple sclerosis (MS) and psoriasis; however, its role in RA is unknown. DMF has immunomodulatory properties and may be considered as therapeutic approach in RA treatment. In this study, we aimed to investigate the effect of DMF on controlling FLS-mediated synovial inflammation and joint destruction in RA. FLSs were isolated from synovial tissues of 8 patients with RA and treated with DMF. Apoptosis rate was analyzed by Annexin V-FITC. Cell proliferation was measured by carboxyfluorescein succinimidyl ester (CFSE) dye. The matrix metalloproteinase 3 (MMP3) and NF-кB pathway protein (p65) mRNA expression were evaluated by RT-PCR. Also, the IL-6 production and lactate release were measured in FLS supernatant. DMF treatment decreased the cell proliferation and increased apoptosis in a dose dependent manner. DMF-treated FLS showed a reduction in IL-6 and lactate release. Moreover, it was revealed that DMF inhibited the expression of p65 and MMP3. Our data demonstrate that DMF treatment suppresses the aggressive and inflammatory features of RA FLSs. Our Results suggest that DMF might be expected to be evaluated as a therapy for RA.

Indexed as

Arthritis, RheumatoidSynoviocytesCell ProliferationCells, CulturedDimethyl FumarateFibroblastsHumansInflammationInterleukin-6Matrix Metalloproteinase 3Synovial MembraneDimethyl FumarateInterleukin-6Matrix Metalloproteinase 3dimethyl fumarate.fibroblast like synoviocyteinflammationrheumatoid arthritis

Identifiers

PMID36253500
OpenAlexW4306640279

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.