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基于高通量测序技术的切口疝转录组分析。

A transcriptomic analysis of incisional hernia based on high-throughput sequencing technology.

机构信息

Department of General Surgery, Fudan University Affiliated Huadong Hosptial, No.221, West Yan'an Road, Jing'an District, Shanghai, 200040, Republic of China.

出版信息

Hernia. 2024 Oct;28(5):1899-1907. doi: 10.1007/s10029-024-03116-7. Epub 2024 Jul 29.

Abstract

PURPOSE

Incisional hernia is a common postoperative complication; however, few transcriptomic studies have been conducted on it. In this study, we used second-generation high-throughput sequencing to explore the pathogenesis and potential therapeutic targets of incisional hernias.

METHODS

Superficial fasciae were collected from 15 patients without hernia and 21 patients with an incisional hernia. High-throughput sequencing of the fascia was performed to generate an expression matrix. We analyzed the matrix to identify differentially expressed genes (DEGs) and performed gene ontology and enrichment analyses of these DEGs. Additionally, an external dataset was utilized to identify key DEGs.

RESULTS

We identified 1,823 DEGs closely associated with extracellular matrix (ECM) imbalance, bacterial inflammatory response, and fibrillar collagen trimerization. TNNT3, CMAY5, ATP1B4, ASB5, CILP, SIX4, FBN1 and FNDC5 were identified as key DEGs at the intersection of the two expression matrices. Moreover, non-alcoholic fatty liver disease-related, TNF, and IL-17 signaling pathways were identified as key enrichment pathways.

CONCLUSIONS

We identified eight key DEGs and three pathways associated with incisional hernias. Our findings offer new insights into the pathogenesis of incisional hernias and highlight potential targets for their prevention and treatment.

摘要

目的

切口疝是一种常见的术后并发症,但关于其发病机制的转录组学研究较少。本研究采用第二代高通量测序技术,探讨切口疝的发病机制和潜在的治疗靶点。

方法

收集 15 例无疝和 21 例切口疝患者的浅筋膜,进行高通量测序以生成表达矩阵。我们分析该矩阵以识别差异表达基因(DEGs),并对这些 DEGs 进行基因本体论和富集分析。此外,还利用外部数据集来识别关键 DEGs。

结果

我们确定了 1823 个与细胞外基质(ECM)失衡、细菌炎症反应和纤维胶原三聚化密切相关的 DEGs。TNNT3、CMAY5、ATP1B4、ASB5、CILP、SIX4、FBN1 和 FNDC5 被确定为两个表达矩阵交集处的关键 DEGs。此外,非酒精性脂肪性肝病相关、TNF 和 IL-17 信号通路被确定为关键富集通路。

结论

我们确定了 8 个关键 DEGs 和 3 个与切口疝相关的通路。我们的研究结果为切口疝的发病机制提供了新的见解,并突出了其预防和治疗的潜在靶点。

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