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Updated: Aug 17, 2025

Optimized Protocol for the Extraction of Proteins from the Human Mitral Valve
Published on: June 14, 2017
Functional analysis of differently expressed ferroptosis-related genes in patients with mitral valve prolapse
Hui Xie1, Liushun Wang1, Yihu Tang1
1Department of Cardiovascular Surgery, Nanjing Medical University First Affiliated Hospital, Nanjing, China.
Abstract:
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.
Insights
Mitral valve prolapse (MVP) pathogenesis involves ferroptosis-related genes and long non-coding RNAs (lncRNAs). Key genes CDKN2A, SLC1A4, and ATF3 identified as potential therapeutic targets for MVP.
Area of Science:
- Cardiovascular Biology
- Molecular Genetics
- Disease Pathogenesis
Background:
- Mitral valve prolapse (MVP) is a growing global health concern within valvular heart diseases.
- Current understanding of MVP's etiology and pathogenesis remains limited.
- The interplay between ferroptosis-related genes and long non-coding RNAs (lncRNAs) in MVP is largely unexplored.
Purpose of the Study:
- To investigate the role of ferroptosis-related genes in the pathogenesis of mitral valve prolapse (MVP).
- To identify potential therapeutic targets for MVP based on gene expression analysis.
- To explore the regulatory network of ferroptosis-related genes and lncRNAs in MVP.
Main Methods:
- Transcriptomic sequencing of blood samples from MVP patients and healthy controls.
- Analysis of differentially expressed genes (DEGs) and differentially expressed lncRNAs (DElncRNAs).
- Construction of a co-expression network and Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses.
Main Results:
- Identification of core ferroptosis-related genes CDKN2A, SLC1A4, and ATF3 associated with MVP.
- These core genes are central in a regulatory network modulated by numerous lncRNAs.
- Enrichment analysis revealed involvement in the extracellular region and p53 signaling pathway.
Conclusions:
- CDKN2A, SLC1A4, and ATF3 are implicated in the pathophysiological processes of MVP.
- These genes represent promising therapeutic targets for mitral valve prolapse.
- Understanding the lncRNA regulation of these genes offers new insights into MVP mechanisms.
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