ArticleJournal of inflammation research2024
Clinical Significance of Abnormal Serum LGALS3BP Expression in Patients with Idiopathic Inflammatory Myopathies.
Article in Journal of inflammation research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed.
- TET1 deficiency amplifies macrophage inflammatory signaling associated with Crohn's disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Idiopathic inflammatory myopathies (IIM) are classified into four subgroups: dermatomyositis (DM), anti-synthetase syndrome (ASS), immune-mediated necrotizing myopathy (IMNM), and sporadic inclusion body myositis (sIBM); however, the role of LGALS3BP in IIM remains unclear. Our study aimed to explore the ability of LGALS3BP to discriminate between the IIM subtypes. The correlation between serum LGALS3BP levels, clinical features, and inflammatory markers in patients with IIM was also assessed. Methods: Based on the Gene Expression Omnibus (GEO) database, we used bioinformatics analysis to screen for overlapping extracellular protein-differentially expressed genes between any two groups of DM, ASS, IMNM, and healthy controls (HCs). This study enrolled 84 patients with IIM and 36 HCs, and participant baseline data and laboratory parameters were recorded. Serum LGALS3BP levels were measured using an enzyme-linked immunosorbent assay (ELISA). Results: Through bioinformatics analysis, LGALS3BP was selected as a potential biomarker for the identification of DM, ASS, IMNM, and HC. LGALS3BP expression decreased sequentially in the DM, ASS, IMNM, and HC groups, with significant differences among the two groups. The ELISA results were similar to those of the bioinformatics analysis; however, the difference in serum LGALS3BP expression between DM and ASS was not statistically significant. According to the receiver operating characteristic (ROC) curve analysis, using HC as the control group, the area under the curve (AUC) values of serum LGALS3BP levels for the diagnosis of IIM, DM, and ASS were > 0.8. In addition, patients with elevated serum LGALS3BP levels had a higher prevalence of interstitial lung disease (ILD). Serum LGALS3BP levels correlated with inflammatory markers. Conclusion: LGALS3BP is differentially expressed in DM, ASS, IMNM, and HC and may assist in assessing the severity of IIM-ILD.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.