Scholarlink

Background <p>Septic-induced coagulopathy (SIC) is a major cause of mortality in sepsis, closely associated with endothelial glycocalyx damage. Enolase 1 (Eno1), a key enzyme in glycolysis, plays a crucial role in sepsis-related systemic inflammation and the maintenance of glycocalyx integrity.</p> Objective <p>This study utilizes multi-omics analysis to investigate the Eno1-regulated network, providing a comprehensive understanding of its molecular mechanisms in SIC.</p> Methods <p>We used RNA-seq datasets to identify Eno1-related gene sets through weighted gene co-expression network analysis and validated their biological functions via gene set enrichment analysis.</p> Results <p>Through RNA-seq analysis, we identified gene sets associated with Eno1 involved in immune regulation, endothelial cell apoptosis, coagulation, and glycosaminoglycan metabolism. Immune infiltration analysis revealed that Eno1 modulates SIC pathogenesis by influencing T cells and macrophages, with significant associations with endothelial dysfunction and inflammatory markers. Additionally, we observed that Eno1 regulation of glycolysis is linked to endothelial glycocalyx degradation, contributing to microcirculatory and vascular impairments in SIC. Furthermore, preliminary studies suggest that melatonin treatment may alleviate glycocalyx damage by inhibiting Eno1-mediated glycolytic pathways, offering a potential new therapeutic avenue for intervening in endothelial injury associated with SIC.</p> Conclusions <p>This study underscores the critical role of Eno1 in promoting SIC and its potential as both a diagnostic marker and therapeutic target for glycocalyx repair. The multi-omics approach provides valuable insights into the molecular networks regulating SIC, offering new avenues for targeted interventions in sepsis management.</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

Eno1 in sepsis-induced coagulopathy: a pleiotropic mechanism hypothesis involving immunomodulation and endothelial dysfunction

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年6月12日

查看全文
  • Ke Qin,
  • Xiao Chen,
  • Xiaoling Li,
  • Wenbin Zhang,
  • Xinnan Song,
  • Yuan Wang,
  • Xiaowen Hu,
  • Jianfeng Zhang

摘要

Background

Septic-induced coagulopathy (SIC) is a major cause of mortality in sepsis, closely associated with endothelial glycocalyx damage. Enolase 1 (Eno1), a key enzyme in glycolysis, plays a crucial role in sepsis-related systemic inflammation and the maintenance of glycocalyx integrity.

Objective

This study utilizes multi-omics analysis to investigate the Eno1-regulated network, providing a comprehensive understanding of its molecular mechanisms in SIC.

Methods

We used RNA-seq datasets to identify Eno1-related gene sets through weighted gene co-expression network analysis and validated their biological functions via gene set enrichment analysis.

Results

Through RNA-seq analysis, we identified gene sets associated with Eno1 involved in immune regulation, endothelial cell apoptosis, coagulation, and glycosaminoglycan metabolism. Immune infiltration analysis revealed that Eno1 modulates SIC pathogenesis by influencing T cells and macrophages, with significant associations with endothelial dysfunction and inflammatory markers. Additionally, we observed that Eno1 regulation of glycolysis is linked to endothelial glycocalyx degradation, contributing to microcirculatory and vascular impairments in SIC. Furthermore, preliminary studies suggest that melatonin treatment may alleviate glycocalyx damage by inhibiting Eno1-mediated glycolytic pathways, offering a potential new therapeutic avenue for intervening in endothelial injury associated with SIC.

Conclusions

This study underscores the critical role of Eno1 in promoting SIC and its potential as both a diagnostic marker and therapeutic target for glycocalyx repair. The multi-omics approach provides valuable insights into the molecular networks regulating SIC, offering new avenues for targeted interventions in sepsis management.