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Updated: Jun 25, 2026

Optimized Protocol for the Extraction of Proteins from the Human Mitral Valve
Published on: June 14, 2017
Molecular Mechanisms in Idiopathic Mitral Valve Chordae Tendineae Rupture: Insights from Transcriptome Analysis and
Qiuji Wang1,2,3, Lishan Zhong1,2, Linbin Hua1,2,3
1Department of Cardiac Surgery, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, 510080, People's Republic of China.
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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