Chen Yilin, Xu Chengfei, Shi Dongchen, Yang Chengcheng, Tong Shulin, Qin Yi, Zhang Wusheng, Li Xiang, Tian Sen, Dong Yuchao, Shi Hui, Bai Chong
Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Naval Medical University, Shanghai, China.
Department of Respiratory and Critical Care Medicine, No. 990 Hospital of the Chinese People's Liberation Army Joint Logistic Support Force, Zhumadian, China.
J Thorac Dis. 2025 Aug 31;17(8):5639-5653. doi: 10.21037/jtd-2024-1987. Epub 2025 Aug 26.
Benign airway stenosis (BAS) is a disease characterized by the formation of fibrotic tissue leading to airway stenosis with unclear underlying molecular mechanisms. This study aimed to identify the key genes regulating fibrosis in BAS.
In this study, the fibrotic mechanism of BAS was explored through combined transcriptomic and proteomic analysis. We collected tracheal samples from day 7 of a mouse model of BAS, as well as from normal control mice. These samples underwent transcriptomic and proteomic sequencing, followed by integrative analysis to identify key genes associated with the condition. Subsequently, we assessed airway fibrosis in the BAS model mice after treatment with an inhibitor targeting the identified gene.
The analysis revealed 4,336 significantly differentially expressed genes (DEGs) at the transcriptomic level and 1,634 differentially expressed proteins (DEPs) at the proteomic level. Through cross-omics integrative analysis, 195 upregulated genes [designated as correlated DEGs and DEPs (cor-DEGs-DEPs)] exhibited significant concordance in expression patterns at both messenger RNA (mRNA) and protein levels, forming differentially co-expressed gene-protein pairs. Utilizing a combined analysis of transcriptomics and proteomics, we identified the gene as a significant factor in this process. Inhibition of was shown to alleviate the fibrotic progression associated with BAS.
may play a key role in the progression of BAS, which may provide a promising therapeutic strategy for BAS.
良性气道狭窄（BAS）是一种以纤维化组织形成为特征的疾病，可导致气道狭窄，其潜在分子机制尚不清楚。本研究旨在确定调节BAS纤维化的关键基因。
在本研究中，通过转录组学和蛋白质组学联合分析来探索BAS的纤维化机制。我们从小鼠BAS模型第7天以及正常对照小鼠中收集气管样本。对这些样本进行转录组学和蛋白质组学测序，随后进行综合分析以鉴定与该疾病相关的关键基因。随后，我们在用靶向鉴定出的基因的抑制剂处理后评估BAS模型小鼠的气道纤维化情况。
分析在转录组水平上揭示了4336个显著差异表达基因（DEG），在蛋白质组水平上揭示了1634个差异表达蛋白质（DEP）。通过跨组学综合分析，195个上调基因[指定为相关DEG和DEP（cor-DEG-DEP）]在信使核糖核酸（mRNA）和蛋白质水平的表达模式上表现出显著一致性，形成差异共表达基因-蛋白质对。利用转录组学和蛋白质组学的联合分析，我们确定该基因是这一过程中的一个重要因素。抑制该基因可减轻与BAS相关的纤维化进展。
该基因可能在BAS进展中起关键作用，这可能为BAS提供一种有前景的治疗策略。
