Functional analysis of differently expressed ferroptosis-related genes in patients with mitral valve prolapse

被引:1
|
作者
Xie, Hui [1 ]
Wang, Liushun [1 ]
Tang, Yihu [1 ]
Zhao, Meng [1 ]
Wang, Zihao [1 ]
Liu, Mingzhu [1 ]
Zhao, Quangong [1 ]
Zhou, Jingxin [1 ]
Wu, Yanhu [1 ]
机构
[1] Nanjing Med Univ, Affiliated Hosp 1, Dept Cardiovasc Surg, Nanjing, Peoples R China
关键词
valve disease; mitral value prolapse; ferroptosis; lncRNA; gene; CANCER; TISSUE;
D O I
10.3389/fgene.2022.1062212
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Background: The prevalence of mitral valve prolapse (MVP) in heart valvular diseases is globally increasing. However, the understanding of its etiology and pathogenesis is limited. So far, the relationship between ferroptosis-related genes and long non-coding RNAs (lncRNAs) in MVP remains unexplored. This study investigates the potential pathogenesis of ferroptosis-related genes in MVP and provides a therapeutic target for the disease. Methods: Blood samples from patients with MVP and healthy volunteers were collected for transcriptomic sequencing to analyze the expression of ferroptosis-related differentially expressed genes (DEGs) and differentially expressed long non-coding RNAs (DElncRNAs Co-expression network of ferroptosis-related DEGs and DElncRNAs. Furthermore, this work conducted GO and KEGG enrichment analyses. Results: CDKN2A, SLC1A4, ATF3, and other core genes related to the mitral valve prolapse were screened out. CDKN2A, SLC1A4, and ATF3 genes were at the core position of the network, regulated by numerous lncRNAs. Notably, these genes are primarily involved in the extracellular region and p53 signaling pathway. Conclusion: In summary, CDKN2A, SLC1A4, and ATF3 regulate the pathophysiological process of MVP and are potential therapeutic targets.
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页数:9
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