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<p>Central airway stenosis, arising from both benign and malignant etiologies, remains challenging to treat effectively. Elucidating the underlying molecular mechanisms is therefore essential.&#xa0;We integrated single-cell RNA sequencing with bulk transcriptomic data to identify key mechanisms in airway stenosis. Findings were subsequently validated using molecular biology assays.&#xa0;Fibroblasts were identified as key contributors to fibrotic remodeling in stenotic airways. Four genes—FAM118A, RCN3, PCSK7, and REEP3—were found to promote airway stenosis. Elevated immune activity was observed in stenotic tissues and showed a positive correlation with the expression of these genes. Mechanistically, these genes facilitate stenosis by activating KRAS→PI3K-AKT pathway, leading to upregulation of fibroblast activation markers. The expression of these genes is transcriptionally regulated by TBX20. Specifically, the ILF3-AS1/miR-212-5p axis regulates FAM118A, PCSK7, and REEP3, but not RCN3.&#xa0;This study&#xa0;aims to provide insights into the pathological mechanisms underlying airway stenosis, with all findings experimentally validated through integrated molecular and cellular approaches.</p>

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Integrating single-cell and bulk RNA-Seq to unravel the molecular mechanisms of airway stenosis

  • 期刊论文

  • 发表日期：

    2025年12月23日

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  • Cheng Xue,
  • Wanyu Wang,
  • Qihong Zhuang,
  • Yihua Lin,
  • Yiming Zeng

摘要

Central airway stenosis, arising from both benign and malignant etiologies, remains challenging to treat effectively. Elucidating the underlying molecular mechanisms is therefore essential. We integrated single-cell RNA sequencing with bulk transcriptomic data to identify key mechanisms in airway stenosis. Findings were subsequently validated using molecular biology assays. Fibroblasts were identified as key contributors to fibrotic remodeling in stenotic airways. Four genes—FAM118A, RCN3, PCSK7, and REEP3—were found to promote airway stenosis. Elevated immune activity was observed in stenotic tissues and showed a positive correlation with the expression of these genes. Mechanistically, these genes facilitate stenosis by activating KRAS→PI3K-AKT pathway, leading to upregulation of fibroblast activation markers. The expression of these genes is transcriptionally regulated by TBX20. Specifically, the ILF3-AS1/miR-212-5p axis regulates FAM118A, PCSK7, and REEP3, but not RCN3. This study aims to provide insights into the pathological mechanisms underlying airway stenosis, with all findings experimentally validated through integrated molecular and cellular approaches.