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特发性二尖瓣腱索断裂的分子机制:来自转录组分析和炎症评估的见解
Authors Wang Q, Zhong L, Hua L, Pang S , Li Y, Zhang Z, Zhao J, Huang H
Received 20 December 2024
Accepted for publication 29 March 2025
Published 5 April 2025 Volume 2025:18 Pages 4771—4783
DOI http://doi.org/10.2147/JIR.S510525
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Prof. Dr. Kattepura Krishnappa Dharmappa
Qiuji Wang,1– 3,* Lishan Zhong,1,2,* Linbin Hua,1– 3 Shanwen Pang,1– 3 Yuxin Li,1,2 Zhaolong Zhang,1,2 Junfei Zhao,1,2 Huanlei Huang1– 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; 2Guangdong Cardiovascular Institute, Guangzhou, 510030, People’s Republic of China; 3Guangdong Provincial Key Laboratory of South China Structural Heart Disease, Guangzhou, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Huanlei Huang, Department of Cardiac Surgery, Guangdong Provincial People’s Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, 106 Zhongshan Second Road, Yuexiu District, Guangzhou, Guangdong, People’s Republic of China, Email hhuanlei@hotmail.com Junfei Zhao, Department of Cardiac Surgery, Guangdong Provincial People’s Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, 106 Zhongshan Second Road, Yuexiu District, Guangzhou, Guangdong, People’s Republic of China, Email zhaojunfei@gdph.org.cn
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.
Keywords: mitral valve prolapse, chordae tendineae rupture, inflammation, immune response, transcriptome, bioinformatics