ArticleAmerican journal of translational research2020
iTRAQ quantitative proteomic analysis differentially expressed proteins and signal pathways in henoch-schönlein purpura nephritis.
Article in American journal of translational research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Research progress on biomarkers of immunoglobulin a vasculitis nephritis: from classical molecules to multi-omics system analysis.Frontiers in immunology · 2026Review
- The biological basis of Blood-Heat syndrome in children with Henoch-Schonlein purpura nephritis: a multidimensional analysis based on clinical proteomics and an animal model.Frontiers in pharmacology · 2026Article
- Advances in multi-omics and therapeutic studies of Henoch-Schönlein purpura.Italian journal of pediatrics · 2025Review
- Exploring the Proteomic Landscape of Cochlear Implant Trauma: An iTRAQ-Based Quantitative Analysis Utilizing an Ex Vivo Model.Journal of clinical medicine · 2025Article
- Biomarker research for Henoch-Schönlein purpura nephritis based on "omics" techniques.Frontiers in medicine · 2025Review
- AZGP1 as a potential biomarker of IgA vasculitis with nephritis in a children‑based urinary proteomics study by diaPASEF.Molecular medicine reports · 2023Article
- Identification of key genes and imbalance of immune cell infiltration in immunoglobulin A associated vasculitis nephritis by integrated bioinformatic analysis.Frontiers in immunology · 2023Article
- Lipid metabolism contribute to the pathogenesis of IgA Vasculitis.Diagnostic pathology · 2022Article
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Authors and funding
5 authors.
Funding
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Abstract
Henoch-Schönlein purpura nephritis (HSPN) has been considered as a major cause of chronic renal failure in children and a condition which can worsen clinical outcomes in adults. At present, the molecular mechanisms of HSPN are still unclear. In this study, iTRAQ quantitative proteomic analysis was performed on renal tissues collected from patients with HSPN and compared with those of patients after nephrectomy (controls). A total of 149 differentially expressed proteins (DEPs) were detected, of which, 97 being upregulated and 52 down-regulated. Protein functions and classifications were analyzed using Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG). In addition, protein domains. expressive hierarchical clustering analysis and protein-protein interaction (PPI) analysis were also conducted for DEPs. The results of bioinformatics analysis indicated that DEPs were enriched in lipid metabolism and the adherens junction pathway. Among these proteins, CDC42 and CTNNB1 were identified as potential candidates involved in the pathogenesis of HSPN. Immunohistochemistry and real-time PCR further demonstrated that CDC42 and CTNNB1 were up-regulated in HSPN patients. These results provide new and important insights into some underlying molecular pathogenesis of HSPN.
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33437369PMC7791518What OpenQuestion holds
Registered trials
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