Scholarlink

Background <p>Chronic rhinosinusitis with nasal polyps (CRSwNP) is a persistent inflammatory airway disease characterized by high recurrence rates despite medical therapy and surgery. The molecular mechanisms underlying disease progression and treatment failure remain incompletely understood, limiting the development of targeted therapies. Transcriptomic studies provide an opportunity to systematically uncover dysregulated genes and pathways involved in CRSwNP pathogenesis.</p> Methods <p>A systematic review was conducted according to PRISMA guidelines across PubMed, Scopus, EMBASE, ScienceDirect, and Web of Science to identify transcriptomics-based case–control studies investigating gene expression in human CRSwNP tissues. Differentially expressed genes (DEGs) reported in eligible studies were compiled and subjected to functional enrichment analysis using Gene Ontology tools. Gene–disease associations with asthma were explored using DisGeNET, and potential drug–gene interactions were identified through DGIdb.</p> Results <p>Fourteen studies comprising 577 samples met the inclusion criteria, yielding 1495 DEGs, of which 70 were experimentally validated. Functional enrichment analysis identified ten significantly dysregulated biological processes, including blood vessel morphogenesis, calcium ion transport, ERK1/ERK2 cascade, intracellular cation homeostasis, regulation of angiogenesis, regulation of actin cytoskeleton organization, and MAPK cascade signaling. Comparative analysis with asthma-associated genes identified 43 shared genes with high confidence. Several genes, including IL4R, IL6R, CSF3, ICAM1, MBL2, SOD1, SCGB1A1, and TSLP, demonstrated interactions with approved or investigational drugs, highlighting potential repurposing opportunities.</p> Conclusions <p>This systematic transcriptomic integration identifies key biological pathways and druggable targets involved in CRSwNP pathogenesis. These findings provide a molecular framework for understanding disease mechanisms and support the development of pathway-oriented and personalized therapeutic strategies in CRSwNP.</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

A systematic review of mRNA alteration and pathway dysregulation in chronic rhinosinusitis with nasal polyp

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年4月29日

查看全文
  • Nasibeh Khayer,
  • Fatemeh Faraji,
  • Mohammad Yousefi,
  • Morteza Fallahpour,
  • Zahra Aazd,
  • Maryam Jalessi,
  • Sara Minaeian

摘要

Background

Chronic rhinosinusitis with nasal polyps (CRSwNP) is a persistent inflammatory airway disease characterized by high recurrence rates despite medical therapy and surgery. The molecular mechanisms underlying disease progression and treatment failure remain incompletely understood, limiting the development of targeted therapies. Transcriptomic studies provide an opportunity to systematically uncover dysregulated genes and pathways involved in CRSwNP pathogenesis.

Methods

A systematic review was conducted according to PRISMA guidelines across PubMed, Scopus, EMBASE, ScienceDirect, and Web of Science to identify transcriptomics-based case–control studies investigating gene expression in human CRSwNP tissues. Differentially expressed genes (DEGs) reported in eligible studies were compiled and subjected to functional enrichment analysis using Gene Ontology tools. Gene–disease associations with asthma were explored using DisGeNET, and potential drug–gene interactions were identified through DGIdb.

Results

Fourteen studies comprising 577 samples met the inclusion criteria, yielding 1495 DEGs, of which 70 were experimentally validated. Functional enrichment analysis identified ten significantly dysregulated biological processes, including blood vessel morphogenesis, calcium ion transport, ERK1/ERK2 cascade, intracellular cation homeostasis, regulation of angiogenesis, regulation of actin cytoskeleton organization, and MAPK cascade signaling. Comparative analysis with asthma-associated genes identified 43 shared genes with high confidence. Several genes, including IL4R, IL6R, CSF3, ICAM1, MBL2, SOD1, SCGB1A1, and TSLP, demonstrated interactions with approved or investigational drugs, highlighting potential repurposing opportunities.

Conclusions

This systematic transcriptomic integration identifies key biological pathways and druggable targets involved in CRSwNP pathogenesis. These findings provide a molecular framework for understanding disease mechanisms and support the development of pathway-oriented and personalized therapeutic strategies in CRSwNP.