ArticleJournal of inflammation research2025
Molecular Mechanisms in Idiopathic Mitral Valve Chordae Tendineae Rupture: Insights from Transcriptome Analysis and Inflammation Evaluation.
Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: This study investigates the molecular mechanisms and hub genes in idiopathic rupture of mitral valve chordae tendineae (iRCT). Methods: Histological changes were assessed via pathological staining, and transcriptome sequencing was performed on samples from 8 iRCT patients and 6 controls. Differentially expressed genes (DEGs), functional enrichment, PPI networks, and immune cell infiltration were analyzed. Hub gene expression was validated using RT-qPCR. Results: iRCT samples exhibited cell proliferation, disorganized collagen fibers, and elastin fiber rupture. Immunohistochemical analysis further confirmed that activated fibroblasts, macrophages, dendritic cells, and T cells were increased in iRCT samples compared to normal samples. Additionally, iRCT samples exhibited an increased content of collagen fibers and elastin fibers. Transcriptome analysis identified 208 DEGs (109 upregulated, 99 downregulated) linked to inflammation, immune activation, and extracellular matrix remodeling. Conclusion: iRCT involves ECM remodeling, inflammation, and immune dysregulation, with identified hub genes offering potential therapeutic targets.
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