ArticlePeerJ2025
Elevated SLC1A5 links to inflamed endothelial cells and proteinuria in membranous nephropathy patients.
Article in PeerJ, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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12 authors.
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Abstract
Background: Membranous nephropathy (MN) is an autoimmune glomerular disorder characterized by persistent proteinuria. Elucidating its pathophysiological mechanisms and signaling pathways is crucial for improving diagnostic and therapeutic strategies. Methods: We performed differential analysis on the MN glomerular transcriptome and assessed immune infiltration. Single-cell analysis identified key genes' subcellular localization, while pseudotime and cell communication analyses determined subpopulations linked to MN progression. Genes causally related to MN onset were screened using Mendelian randomization, and serum core genes were correlated with proteinuria Results: Transcriptome analysis revealed 95 differentially expressed genes, predominantly enriched in immune and metabolic pathways. Macrophage polarization played a pivotal role in MN, with monocytes/macrophages and endothelial cells identified as key contributors. Pseudotemporal analysis showed elevated pro-inflammatory macrophages and inflammatory endothelial cells in high-proteinuria patients. Macrophage-endothelial cell communication involved key signaling molecules. hdWGCNA analysis identified three molecular sets linked to inflammatory cells, with Mendelian randomization confirming their causal relationship to MN. SLC1A5 was identified as a key gene, and serum sample validation confirmed its strong correlation with proteinuria. Conclusion: This study identified novel macrophage and endothelial cell subtypes and their interactions, positioning SLC1A5 as a potential biomarker for MN pathogenesis.
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