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Submitted: 10 Nov 2025
Revision: 22 Dec 2025
Accepted: 18 Apr 2026
ePublished: 20 May 2026
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Immunopathol Persa. Inpress.
doi: 10.34172/ipp.2025.44012
  Abstract View: 4

Original

Uncovering molecular mechanisms and therapeutic targets in systemic lupus erythematosus through integrative transcriptomic and network-based analysis

Mozhdeh Ghamari 1 ORCID logo, Arman Hosseini 2, Forouzan Amerizadeh 3,4* ORCID logo

1 Rheumatic Diseases Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
2 Student Research Committee, Mashhad University of Medical Sciences, Mashhad, Iran
3 Cancer Molecular Pathology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
4 Department of Internal Medicine, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
*Corresponding Author: Forouzan Amerizadeh, Email: amerizadehf4011@mums.ac.ir, Email: amerizadehf951@gmail.com

Abstract

Introduction: Systemic lupus erythematosus (SLE) is a multifactorial autoimmune disorder with heterogeneous clinical manifestations and limited specific biomarkers. Advances in transcriptomic profiling offer an opportunity to dissect underlying molecular mechanisms and identify therapeutic targets.

Objectives: To perform a comprehensive bioinformatics analysis of gene expression profiles in peripheral blood of SLE patients and to identify differentially expressed genes (DEGs), functional pathways, key regulatory genes (hub genes), and druggable targets.

Materials and Methods: This is an in-silico study based on gene expression data (GSE17755) from 10 SLE patients and 20 healthy controls were analyzed using GEO2R. DEGs were subjected to functional enrichment analysis [Gene ontology (GO) and Reactome], protein-protein interaction (PPI) network construction (STRING, Cytoscape), hub gene identification (CytoHubba), cluster detection (ClusterONE), and drug-target interaction mapping (DrugBank).

Results: A total of 1,450 DEGs were identified between SLE patients and healthy controls. Gene ontology and Reactome analyses highlighted enrichment in innate immune responses, interferon signaling, and cytokine-mediated pathways. Thirteen key hub genes including GAPDH, PTEN, PTPRC, UBA52, and ISG15 were identified across multiple centrality metrics. ClusterONE detected significant modules enriched in immune-related genes, ribosomal proteins, keratin family genes, and transcription factors. Drug-target analysis revealed GAPDH as the most connected node, interacting with compounds like artenimol, omigapil, and xanthinol, indicating potential avenues for drug repurposing.

Conclusion: Our integrative analysis highlighted interferon signaling, cytokine-mediated pathways, and innate immune responses as central mechanisms in SLE. Drug–target mapping suggested several compounds, including artenimol, omigapil, NADH, 4-(2-aminoethyl) benzenesulfonyl fluoride, xanthinol, copper, and phosphatidylethanolamine, as potential modulators of key hub genes. These findings provide preliminary hypotheses that may guide future research; however, additional validation in molecular (in-vitro) experiments and animal (in-vivo) models is required before any translational application can be considered.


Citation: Ghamari M, Hosseini A, Amerizadeh F. Uncovering molecular mechanisms and therapeutic targets in systemic lupus erythematosus through integrative transcriptomic and network-based analysis. Immunopathol Persa. 2026;x(x):e44012. DOI:10.34172/ipp.2025.44012.
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