Evidence map›Paper›PMID 41493486›Full record

ArticleInflammation2026

Metrnl/Meteorin-like/IL-41 Alleviates Rheumatoid Arthritis Via PPARγ-Mediated Suppression of Inflammation, Angiogenesis, and Bone Destruction.

Tao Sun, Liping Xia, Yuxuan Li, Min Zhao, Zhuoqi Li, Hui Shen

Abstract read
In one paragraph

Article in Inflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–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

1 citing paper in PubMed.

  1. Article
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

6 authors.

Tao SunDepartment of Rheumatology and Immunology, The First Hospital of China Medical University, China Medical University, Shen Yang, 110002, China.
Liping XiaDepartment of Rheumatology and Immunology, The First Hospital of China Medical University, China Medical University, Shen Yang, 110002, China.
Yuxuan LiDepartment of Rheumatology and Immunology, Shengjing Hospital of China Medical University, China Medical University, Shen Yang, 110004, China.
Min ZhaoNational Clinical Research Center for Laboratory Medicine, Department of Laboratory Medicine, The First Hospital of China Medical University, Shenyang, 110002, China.
Zhuoqi LiDepartment of Rheumatology and Immunology, The First Hospital of China Medical University, China Medical University, Shen Yang, 110002, China. lzq06060808@163.com.
Hui ShenDepartment of Rheumatology and Immunology, The First Hospital of China Medical University, China Medical University, Shen Yang, 110002, China. shenhuicam@sohu.com.

Funding

Department of Science and Technology of Liaoning Province 2024JH2/102600314
6 · The paper itself

Abstract

Rheumatoid arthritis (RA), an autoimmune disease, is characterized by synovial hyperplasia, vascular occlusion, and bone erosion. Metrnl, a novel secreted protein linked to inflammatory immune regulation, has been implicated in RA pathogenesis, but its precise mechanisms remain undefined. This study aimed to elucidate Metrnl's role in RA progression and therapeutic potential. Proteomic analysis was employed to assess Metrnl's direct effects on RA fibroblast-like synoviocytes (RA-FLS). In vitro, LPS-induced RA-FLS were treated with Metrnl to evaluate proliferation, apoptosis, cell cycle progression, and expression of inflammatory cytokines (IL-6, IL-17, TNF-α) and angiogenic factors (PDGF, VEGF) via PPARγ signaling. Collagen-induced arthritis (CIA) mice models were established to validate therapeutic efficacy, with Micro-CT and histology quantifying joint damage and inflammation. Proteomics results indicated Metrnl's multidirectional role in coordinating vascular homeostasis and immune-inflammatory network activation. Molecular biological results showed that Metrnl suppressed proliferation, promoted apoptosis, and downregulated IL-6, IL-17, TNF-α, PDGF, and VEGF through PPARγ in LPS-induced RA-FLS cells. In CIA mice, Metrnl mitigated weight loss, reduced swollen joints, and improved behavioral scores. Micro-CT confirmed attenuated cartilage/bone destruction and joint deformities, while histology revealed diminished inflammatory infiltration. Metrnl exerts anti-inflammatory and anti-angiogenic effects in RA by modulating PPARγ signaling, highlighting its dual role in suppressing synovitis and vascular remodeling. These findings propose Metrnl as a novel therapeutic target to impede RA progression, offering insights into its pathological mechanisms. Furthermore, Metrnl mitigates bone erosion and joint deformities, underscoring its broader translational potential for treating bone-related disorders.

Indexed as

Arthritis, ExperimentalArthritis, RheumatoidInterleukinsNeovascularization, PathologicPPAR gammaAngiogenesisAnimalsApoptosisHumansInflammationMiceMice, Inbred DBASignal TransductionSynoviocytesInterleukinsPPAR gammaAngiogenesisCytokineInflammationMetrnlRheumatoid arthritis

Identifiers

PMID41493486
PMCPMC12832592

What Socratic 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 Socratic graph.