ArticleLupus science & medicine2025
Proteomics uncovers ICAM2 (CD102) as a novel serum biomarker of proliferative lupus nephritis.
Article in Lupus science & medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Clerodendrum japonicum Extract Suppresses the Pathogenicity of Rheumatoid Arthritis Fibroblast-Like Synoviocytes by Inhibiting METTL3-Mediated ICAM2 mRNA Methylation.Cell biochemistry and function · 2026Article
- Biomarkers in Lupus Nephritis: An Evidence-Based Comprehensive Review.Life (Basel, Switzerland) · 2025Review
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11 authors.
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Abstract
objectivesThis study aimed to identify novel, non-invasive biomarkers for lupus nephritis (LN) through serum proteomics.
methodsSerum proteins were detected in patients with LN and healthy control (HC) groups through liquid chromatography-tandem mass spectrometry. The key networks associated with LN were screened out using Cytoscape software, followed by pathway enrichment analysis. The best candidate biomarkers were selected by machine learning models, further validated in a larger independent cohort. Finally, the expression of these candidate markers was verified in kidney tissue samples, and the mechanism was explored by knocking down the expression of intercellular adhesion molecule 2 (ICAM2) through in vitro cell transfection with siRNA.
resultsFollowing the serum proteomic screening of LN, a key network of 20 proteins was identified. Machine learning models were used to select ICAM2 (CD102), metalloproteinase inhibitor 1 (TIMP1) and thrombospondin 1 (THSB1) for validation in independent cohorts. ICAM2 exhibited the highest area under the curve (AUC) value in distinguishing LN from HC (AUC=0.92) and was significantly correlated with activity index, proteinuria, albumin and anti-dsDNA antibody levels. Particularly, ICAM2 was significantly elevated in proliferative LN and was associated with specific pathological attributes, outperforming conventional parameters in distinguishing proliferative LN from non-proliferative LN. ICAM2 expression was also elevated in renal tissue samples from patients with proliferative LN. In vitro, knockdown of ICAM2 expression can inhibit the activation of the PI3K/Akt pathway and alleviate the injury of glomerular endothelial cells.
conclusionICAM2 (CD102) may serve as a potential serum biomarker for proliferative LN that reflects renal pathology activity, potentially contributing to the progression of LN through the PI3K/Akt pathway.
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