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ETS2基因在炎症性肠病中的作用:一篇叙述性综述。

Role of ETS2 gene in inflammatory bowel disease: A narrative review.

作者信息

Aakash F N U, Kumar Sunny, Kumari Aasta, Shweta F N U, Rumela F N U, Partab F N U, Singla Shivam, Parveen Abida

机构信息

Department of Medicine, Ibn e Seena Hospital, Kabul, Afghanistan.

出版信息

Medicine (Baltimore). 2025 Sep 5;104(36):e44234. doi: 10.1097/MD.0000000000044234.

Abstract

The ETS2 gene, a member of the ETS (E26 transformation-specific) family of transcription factors, plays a critical role in the regulation of immune responses, epithelial barrier integrity, and fibrosis, all of which are central to the pathogenesis of inflammatory bowel disease (IBD). This review explores the molecular characteristics of ETS2, its involvement in immune dysregulation, and its contribution to IBD-associated complications, including fibrosis and colorectal cancer. ETS2 regulates key inflammatory pathways such as NF-κB and JAK-STAT, influencing cytokine production and immune cell polarization. Additionally, it affects epithelial barrier function by modulating tight junction proteins, thereby impacting intestinal permeability. Dysregulation of ETS2 expression can exacerbate intestinal inflammation, promote fibrosis, and increase the risk of colorectal cancer in IBD patients. Genetic variants of ETS2 have been associated with disease susceptibility, suggesting its potential as a biomarker for disease progression. Furthermore, targeting ETS2 may provide novel therapeutic strategies for IBD by modulating inflammatory pathways, restoring epithelial integrity, and preventing fibrosis and cancer. Understanding the role of ETS2 in IBD pathogenesis could lead to more personalized treatment approaches and improved clinical outcomes. This review highlights the potential of ETS2 as a therapeutic target and underscores the need for further research to elucidate its precise molecular mechanisms in IBD.

摘要

ETS2基因是ETS(E26转化特异性)转录因子家族的成员之一,在免疫反应调节、上皮屏障完整性和纤维化过程中发挥关键作用,而这些过程对于炎症性肠病(IBD)的发病机制都至关重要。本综述探讨了ETS2的分子特征、其在免疫失调中的作用以及对IBD相关并发症(包括纤维化和结直肠癌)的影响。ETS2调节关键的炎症信号通路,如NF-κB和JAK-STAT,影响细胞因子的产生和免疫细胞极化。此外,它通过调节紧密连接蛋白来影响上皮屏障功能,从而影响肠道通透性。ETS2表达失调会加剧肠道炎症,促进纤维化,并增加IBD患者患结直肠癌的风险。ETS2的基因变异与疾病易感性相关,表明其作为疾病进展生物标志物的潜力。此外,靶向ETS2可能通过调节炎症信号通路、恢复上皮完整性以及预防纤维化和癌症,为IBD提供新的治疗策略。了解ETS2在IBD发病机制中的作用可能会带来更个性化的治疗方法并改善临床结果。本综述强调了ETS2作为治疗靶点的潜力,并强调需要进一步研究以阐明其在IBD中的精确分子机制。

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