ArticleArthritis & rheumatology (Hoboken, N.J.)2026
Unveiling Endotypes in Systemic Lupus Erythematosus Through Multiomic Analysis: Insights Into Cardiovascular and Renal Complications.
Article in Arthritis & rheumatology (Hoboken, N.J.), 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
23 authors.
Funding
Abstract
objectiveSystemic lupus erythematosus (SLE) shows clinical and molecular heterogeneity, and cardiovascular (CV) complications and lupus nephritis (LN) remain leading causes of morbidity and mortality. This study investigated whether omic profiling can reveal molecular endotypes linked to these outcomes.
methodsSerum from 199 patients with SLE underwent proximity extension assay-based proteomics and targeted nuclear magnetic resonance metabolomics. Unsupervised clustering was performed on proteomic data, followed by integrative multiomic factor analysis, logistic regression, and machine learning models. Cohorts with SLE from the University College London, a subset with expanded Olink Reveal panel and untargeted metabolomics, and in vitro (human umbilical vein endothelial cell and HK2) and ex vivo (rat kidneys) models exposed to patient sera were used for validation and mechanistic exploration.
resultsProteomic clustering identified two molecular subgroups (cluster 1 and cluster 2). Compared with cluster 2, cluster 1 showed damage burden and increased rates of LN (1.8-fold), hypertension (3-fold), dyslipidemia (2-fold), obesity (8-fold), and abnormal C-reactive protein/erythrocyte sedimentation rate (4-fold), consistent with CV risk. A total of 47 inflammatory and organ-damage proteins and multiple metabolites were increased in cluster 1. Neural network models based on metabolites and clinical variables discriminated clusters (area under the curve = 0.77), highlighting citrate and lipoproteins as key features. Multiomic analyses and external cohorts confirmed reproducibility and enrichment in pathways related to leukocyte trafficking, endothelial stress, and nephritis. In vitro, serum from patients with SLE induced NF-κB activation in rat kidneys compared with controls, supporting a proinflammatory effect.
conclusionMultiomic profiling delineates molecular endotypes in SLE, integrating immune, vascular, and metabolic pathways associated with CV risk and LN, supporting their potential for precision risk stratification.
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.