Scholarlink

Purpose <p>Endometriosis (EM) and recurrent spontaneous abortion (RSA) exhibit clinical associations, yet their shared molecular mechanisms remain unclear. This study aimed to identify shared molecular mechanisms and potential hub genes underlying EM and RSA.</p> Methods <p>Differentially expressed genes (DEGs) were identified from EM (GSE7305) and RSA (GSE165004) datasets. Functional enrichment and weighted gene co-expression network analysis (WGCNA) revealed shared pathways and key modules. Venny software was used to identify hub genes between DEGs and key module genes. The diagnostic value of FXYD1 was assessed via ROC analysis. Regulatory networks and immune cell infiltration were explored. Pan-cancer analysis was conducted to assess FXYD1’s expression profile across tumor types. Single-cell RNA sequencing validated FXYD1 expression in EM tissues, maternal–fetal interface and RSA samples.</p> Results <p>DEGs in EM and RSA were enriched in pathways associated with abnormal proliferation, immune dysfunction, and developmental regulation. FXYD1 was identified as a shared hub gene, upregulated in both conditions, with potential diagnostic value. It was correlated with immune cell populations, particularly natural killer (NK) cells. Pan-cancer analysis revealed widespread FXYD1 downregulation across multiple cancer types. Single-cell RNA sequencing confirmed elevated FXYD1 expression in stromal and decidual cells of RSA tissues, implicating its role in impaired decidualization.</p> Conclusions <p>FXYD1 emerges as a critical molecular link between EM and RSA, potentially contributing to decidualization dysfunction. Its dysregulation may underlie the shared pathophysiology of these conditions, offering new insights into their molecular mechanisms.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Identification of shared pathogenetic mechanisms between endometriosis and RSA based on comprehensive bioinformatics analysis

  • 期刊论文

  • 发表日期：

    2025年7月24日

查看全文
  • Jie Sheng,
  • Yanling Dong,
  • Yao Yuan,
  • Li Zhang,
  • Zhenpeng Sun,
  • Yan Huang,
  • Yingxiong Wang,
  • Siyu Lu

摘要

Purpose

Endometriosis (EM) and recurrent spontaneous abortion (RSA) exhibit clinical associations, yet their shared molecular mechanisms remain unclear. This study aimed to identify shared molecular mechanisms and potential hub genes underlying EM and RSA.

Methods

Differentially expressed genes (DEGs) were identified from EM (GSE7305) and RSA (GSE165004) datasets. Functional enrichment and weighted gene co-expression network analysis (WGCNA) revealed shared pathways and key modules. Venny software was used to identify hub genes between DEGs and key module genes. The diagnostic value of FXYD1 was assessed via ROC analysis. Regulatory networks and immune cell infiltration were explored. Pan-cancer analysis was conducted to assess FXYD1’s expression profile across tumor types. Single-cell RNA sequencing validated FXYD1 expression in EM tissues, maternal–fetal interface and RSA samples.

Results

DEGs in EM and RSA were enriched in pathways associated with abnormal proliferation, immune dysfunction, and developmental regulation. FXYD1 was identified as a shared hub gene, upregulated in both conditions, with potential diagnostic value. It was correlated with immune cell populations, particularly natural killer (NK) cells. Pan-cancer analysis revealed widespread FXYD1 downregulation across multiple cancer types. Single-cell RNA sequencing confirmed elevated FXYD1 expression in stromal and decidual cells of RSA tissues, implicating its role in impaired decidualization.

Conclusions

FXYD1 emerges as a critical molecular link between EM and RSA, potentially contributing to decidualization dysfunction. Its dysregulation may underlie the shared pathophysiology of these conditions, offering new insights into their molecular mechanisms.