Evidence map›Paper›PMID 36694465›Full record

ArticleBioengineered2022

Exosomes derived from fibrinogen-like protein 1-overexpressing bone marrow-derived mesenchymal stem cells ameliorates rheumatoid arthritis.

Wenqiang Xu, Xiaofeng Liu, Wenqing Qu, Xin Wang, Hao Su, Wenliang Li, Yiheng Cheng

RetractedAbstract readRetracted Publication
In one paragraph

Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

15 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  8. Exploring new frontiers in LAG-3 biology and therapeutics.Trends in pharmacological sciences · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors.

Wenqiang XuDepartment of Orthopaedics, the Affiliated Laishan Branch of Yantai Yuhuangding Hospital of Qingdao University, Yantai, Shandong, China.
Xiaofeng LiuDepartment of Traumatic Orthopaedics, the Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, Shandong, China.
Wenqing QuDepartment of Orthopaedics, YanTaiShan Hospital, Yantai, Shandong, China.
Xin WangDepartment of Traumatic Orthopaedics, the Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, Shandong, China.
Hao SuDepartment of Traumatic Orthopaedics, the Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, Shandong, China.
Wenliang LiDepartment of Orthopaedics, YanTaiShan Hospital, Yantai, Shandong, China.
Yiheng ChengDepartment of Orthopaedics, YanTaiShan Hospital, Yantai, Shandong, China.ORCID 0000-0002-2864-4276

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rheumatoid arthritis (RA) is a most common chronic joint disease belonging to inflammatory autoimmune disease. The aim of this study was to determine the role and mechanism of bone marrow mesenchymal stem cells (BMSCs)-derived exosomes and fibrinogen-like protein 1 (FGL1) overexpression exosomes shuttled by BMSCs (FGL1-Exos) on RA. All of the exosomes were visualized by transmission electron microscope (TEM) and the characteristic proteins were detected by western blot. To investigate the therapeutic effect of FGL1-Exos, RA-FLSs were activated by TNF-α and RA rat model was established by collagen incomplete Freund's adjuvant. Cell viability, apoptosis, inflammation factors, and protein levels were detected by CCK-8, flow cytometry, enzyme-linked immunosorbent assay and western blot, respectively. Hematoxylin and eosin and safranin O staining were used to detect the histopathology changes. Cell apoptosis and FGL1 expression in knee joint were detected by immunofluorescence. The results showed that FGL1-Exos could inhibit the cell viability meanwhile increase the cell apoptosis in RA-FLSs. Meanwhile, FGL1-Exos could effectively suppress the inflammation score, joint destruction, and inflammatory response in RA rat model. FGL1-Exos directly inhibited cell apoptosis of RA-FLSs and RA rat model by suppressing the inflammatory cytokines, specific rheumatoid markers, immunological markers meanwhile meditating the NF-κB pathway. Our results indicate that FGL1 was a therapeutic potential target in RA therapy.

Indexed as

Arthritis, RheumatoidExosomesMesenchymal Stem CellsAnimalsBone MarrowFibrinogenInflammationRatsFibrinogenFibrinogen-like protein 1mesenchymal stem cell-derived exosomesNF-κBrheumatoid arthritis

Identifiers

PMID36694465
PMCPMC9995129

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Registered trials

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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.