ArticleComputational and mathematical methods in medicine2020
Systematic Identification of lncRNA-Associated ceRNA Networks in Immune Thrombocytopenia.
Article in Computational and mathematical methods in medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Platelet-derived non-coding RNAs as emerging contributors to autoimmune inflammation.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- The intersection of epigenetics and immune thrombocytopenia: new insights into disease mechanisms and treatments.Molecular biology reports · 2025Review
- Decreased Expression of IL-35 and Its Receptor Contributes to Impaired Megakaryopoiesis in the Pathogenesis of Immune Thrombocytopenia.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Novel Biomarkers for Diagnosis and Monitoring of Immune Thrombocytopenia.International journal of molecular sciences · 2023Review
- Article
- The Construction of ITP Diagnostic Modeling Based on the Expressions of Hub Genes Associated with M1 Polarization of Macrophages.Journal of inflammation research · 2022Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary immune thrombocytopenia (ITP) is an autoimmune disease. However, the molecular mechanisms underlying ITP remained to be further investigated. In the present study, we analyzed a series of public datasets (including GSE43177 and GSE43178) and identified 468 upregulated mRNAs, 272 downregulated mRNAs, 134 upregulated lncRNAs, 23 downregulated lncRNAs, 29 upregulated miRNAs, and 39 downregulated miRNAs in ITP patients. Then, we constructed protein-protein interaction networks, miRNA-mRNA and lncRNA coexpression networks in ITP. Bioinformatics analysis showed these genes regulated multiple biological processes in ITP, such as mRNA nonsense-mediated decay, translation, cell-cell adhesion, proteasome-mediated ubiquitin, and mRNA splicing. We thought the present study could broaden our insights into the mechanism underlying the progression of ITP and provide a potential biomarker for the prognosis of ITP.
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Registered trials
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