ArticleFrontiers in immunology2022
Molecular Taxonomy of Systemic Lupus Erythematosus Through Data-Driven Patient Stratification: Molecular Endotypes and Cluster-Tailored Drugs.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- Myocardial injury in systemic lupus erythematosus and lupus nephritis: a silent threat.Clinical kidney journal · 2026Review
- Artificial Intelligence and Machine Learning in Rheumatology and Systemic Inflammatory Diseases: From Pattern Recognition to Signal Analysis and Clinical Decision Support.Journal of clinical medicine · 2026Review
- Gene Expression as a Guide for the Development of Novel Therapies in Hypertensive and Diabetic Kidney Disease.Journal of clinical medicine · 2026Article
- Applications of artificial intelligence in systemic lupus erythematosus: integrating multi-omics data for precision medicine.Frontiers in immunology · 2026Review
- Immune-cell profiling to guide stratification and treatment of patients with rheumatic diseases.Nature reviews. Rheumatology · 2025Review
- Article
- Data-Driven Cluster Analysis of Cerebrospinal Fluid Proteome and Associations with Clinical Phenotypes in Systemic Lupus Erythematosus.ACR open rheumatology · 2025Article
- Artificial Intelligence in Rheumatology: Quo Vadis?Mediterranean journal of rheumatology · 2025Article
- Neutrophil Heterogeneity Identifies an Association of LAMP1 With Proliferative Lupus Nephritis.European journal of immunology · 2025Article
- Prognostic insights from symptom clustering analysis in systemic lupus erythematosus.RMD open · 2025Article
- Transcriptome analysis to decipher the molecular underpinnings of response to treatment in systemic lupus erythematosus.RMD open · 2025Article
- Systemic lupus erythematosus genetics: insights into pathogenesis and implications for therapy.Nature reviews. Rheumatology · 2024Review
- Analysis of transcriptomic features reveals molecular endotypes of SLE with clinical implications.Genome medicine · 2023Article
- Precision medicine in systemic lupus erythematosus.Nature reviews. Rheumatology · 2023Review
- Restoration of aberrant gene expression of monocytes in systemic lupus erythematosus via a combined transcriptome-reversal and network-based drug repurposing strategy.BMC genomics · 2023Article
- Treatment of lupus nephritis: consensus, evidence and perspectives.Nature reviews. Rheumatology · 2023Review
- The genomic landscape of ANCA-associated vasculitis: Distinct transcriptional signatures, molecular endotypes and comparison with systemic lupus erythematosus.Frontiers in immunology · 2023Article
- Drug Repurposing at the Interface of Melanoma Immunotherapy and Autoimmune Disease.Pharmaceutics · 2022Review
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objectives: Treatment of Systemic Lupus Erythematosus (SLE) is characterized by a largely empirical approach and relative paucity of novel compound development. We sought to stratify SLE patients based on their molecular phenotype and identify putative therapeutic compounds for each molecular fingerprint. Methods: By the use of whole blood RNA-seq data from 120 SLE patients, and in a data-driven, clinically unbiased manner, we established modules of commonly regulated genes (molecular endotypes) and re-stratified patients through hierarchical clustering. Disease activity and severity were assessed using SLEDAI-2K and Lupus Severity Index, respectively. Through an Results: Molecular taxonomy identified five lupus endotypes, each characterized by a unique gene module enrichment pattern. Neutrophilic signature group consisted primarily of patients with active lupus nephritis, while the B-cell expression group included patients with constitutional features. Patients with moderate severity and serologic activity exhibited a signature enriched for metabolic processes. Mild disease was distributed in two groups, exhibiting enhanced basic cellular functions, myelopoiesis, and autophagy. Bortezomib was predicted to reverse disturbances in the "neutrophilic" cluster, azathioprine and ixazomib in the "B-cell" cluster, and fostamatinib in the "metabolic" patient subgroup. Conclusion: The clinical spectrum of SLE encompasses distinct molecular endotypes, each defined by unique pathophysiologic aberrancies potentially reversible by distinct compounds.
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