ArticlePloS one2026
The shared biomarkers and molecular mechanisms of systemic lupus erythematosus and type 2 diabetes.
Article in PloS one, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Systemic lupus erythematosus (SLE) and type 2 diabetes mellitus (T2DM) share inflammatory and metabolic disturbances, yet the molecular mechanism of their overlap remains unclear. This study used integrated bioinformatics to identify transcriptomic signatures and potential biomarkers common to both conditions. Gene expression profiles from publicly available datasets (SLE: 38 patients/32 controls; T2DM: 6 patients/6 controls; validation cohorts: 79/30 and 41/15, respectively) were analyzed to detect shared differentially expressed genes and co-expression modules. Functional enrichment, protein-protein interaction networks, and immune-cell composition analyses were performed. Diagnostic gene panels were constructed using random forest feature selection and logistic regression and evaluated through receiver operating characteristic analysis with external validation. A total of 551 shared differentially expressed genes were identified, enriched predominantly in type I interferon signaling, Toll-like/NOD receptor pathways, TNF signaling, necroptosis, and neutrophil extracellular trap formation. Across analytical methods, a 10-gene interferon-related hub (STAT1, IRF7, OAS1, OAS2, ISG15, MX2, IFI35, RSAD2, SAMD9, SAMD9L) genes demonstrated strong discriminative performance in both SLE and T2DM. A three-gene model further showed potential clinical utility (AUC 0.872-1.00 in discovery; 0.665-0.928 in validation).These signatures align with therapeutic axes in SLE (IFN/JAK-STAT) and intersect inflammatory-metabolic pathways in T2DM, supporting assayable biomarkers and compact diagnostic models that warrant validation in larger, medication-annotated cohorts.
Indexed as
Identifiers
What Socratic 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 Socratic graph.