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Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
Published on: August 23, 2024
Identification of molecular mechanism and key biomarkers in membranous nephropathy by bioinformatics analysis
Zhaocheng Dong1,2, Yunling Geng1,2, Pingna Zhang1,2
1Dongzhimen Hospital, Beijing University of Chinese Medicine Beijing, China.
Objectives:
Membranous nephropathy (MN) is an autoimmune nephropathy. The incidence of MN is increasing gradually in recent years. Previous studies focused on antibody production, complement activation and podocyte injury in MN. However, the etiology and underlying mechanism of MN remain to be further studied.
Methods:
GSE104948 and GSE108109 of glomerular expression profile were downloaded from Gene Expression Omnibus (GEO) database, GSE47184, GSE99325, GSE104954, GSE108112, GSE133288 of renal tubule expression profile, and GSE73953 of peripheral blood mononuclear cells (PBMCs) expression profile. After data integration by Networkanalyst, differentially expressed genes (DEGs) between MN and healthy samples were obtained. DEGs were enriched in gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG), and protein-protein interaction (PPI) networks of these genes were constructed through Metascape, etc. We further understood the function of hub genes through gene set enrichment analysis (GSEA). The diagnostic value of DEGs in MN was evaluated by receiver operating characteristic (ROC) analysis.
Results:
A total of 3 genes (TP53, HDAC5, and SLC2A3) were screened out. Among them, the up-regulated TP53 expression may be closely related to MN renal pathological changes. However, the expression of MN podocyte target antigen was not significantly different from that of healthy controls. In addition, the changes of Wnt signaling pathway in PBMCs and the effects of SLC2A3 on the differentiation of M2 monocyte need further study.
Conclusion:
It is difficult to unify a specific mechanism for the changes of glomerulus, renal tubules and PBMCs in MN patients. This may be related to the pathogenesis, pathology and immune characteristics of MN. MN podocyte target antigen may not be the root cause of the disease, but a stage result in the pathogenesis process.
Insights
Membranous nephropathy (MN) involves complex mechanisms beyond podocyte injury. This study identified TP53, HDAC5, and SLC2A3 as key genes, suggesting a multi-faceted etiology for this autoimmune kidney disease.
Area of Science:
- Nephrology
- Immunology
- Genomics
Background:
- Membranous nephropathy (MN) is an autoimmune kidney disease with increasing incidence.
- Previous research focused on antibody production, complement activation, and podocyte injury.
- The precise etiology and underlying mechanisms of MN require further investigation.
Purpose of the Study:
- To explore the underlying mechanisms and identify key genes involved in membranous nephropathy (MN).
- To analyze gene expression profiles in glomeruli, renal tubules, and peripheral blood mononuclear cells (PBMCs) of MN patients.
- To investigate the diagnostic value of differentially expressed genes (DEGs) in MN.
Main Methods:
- Downloaded glomerular, renal tubule, and PBMC expression profiles from the Gene Expression Omnibus (GEO) database.
- Integrated data and identified DEGs between MN and healthy samples using NetworkAnalyst.
- Constructed protein-protein interaction (PPI) networks and performed Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses.
Main Results:
- Identified three key genes: TP53, HDAC5, and SLC2A3.
- Observed up-regulated TP53 expression potentially linked to renal pathological changes in MN.
- Found no significant difference in MN podocyte target antigen expression compared to controls; noted Wnt signaling pathway changes in PBMCs and SLC2A3's role in M2 monocyte differentiation.
Conclusions:
- A unified mechanism for glomerular, renal tubule, and PBMC changes in MN remains elusive, possibly due to disease pathogenesis, pathology, and immune characteristics.
- MN podocyte target antigen may be a consequence rather than the root cause of the disease.
- Further research is needed to elucidate the roles of Wnt signaling and SLC2A3 in MN pathogenesis.
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