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在肠神经细胞中,FGL2诱导的代谢失调提供了对赫施普朗格病的病原体的洞察

Jichang Han¹, Xiaoyang Liu¹, Yixuan Wang¹

¹Department of Pediatric Surgery, Qilu Hospital of Shandong University, Jinan, China.

|September 22, 2025

概括

纤维素样蛋白2 (FGL2) 在赫施普隆病 (HSCR) 中升高,通过增加氧化应激,促进肠神经细胞 (ENCCs) 的死亡. 这确定了FGL2作为HSCR病变发生的潜在因素.

科学领域:

发育生物学是发展生物学.
胃肠病学胃肠病学
分子生物学分子生物学

背景情况:

赫施普隆病 (Hirschsprung disease,HSCR) 是一种先天性疾病,由肠道部分缺少肠神经细胞 (ENCC) 造成.
在HSCR中ENCC损失背后的精确分子机制仍然不完全理解.

研究的目的:

调查纤维素样蛋白2 (FGL2) 在希尔施普朗格病的发病过程中的作用.
阐明FGL2通过哪些分子途径影响ENCC生存.

主要方法:

从HSCR患者的角质结肠组织中分析FGL2表达.
使用初级小鼠胚胎ENCC进行体外研究,以评估FGL2刺激对细胞亡的影响.
调查JAK2-STAT3信号通路和氧化酸化 (OXPHOS) 作为对FGL2.2的反应.

主要成果:

纤维素样蛋白2 (FGL2) 的表达在HSCR患者的大肠腺组织中显著上调.
在初级ENCC中,FGL2刺激会导致亡的增加.
FGL2激活了JAK2-STAT3通路,增强了OXPHOS,导致反应性氧物种 (ROS) 积累和随后的ENCC亡.

结论:

纤维素样蛋白2 (FGL2) 被确定为希尔施普朗格病的潜在致病因子.
FGL2通过一种涉及增强氧化酸化和ROS生产的机制,对ENCC的生存产生负面影响.
这些发现为HSCR中ENCCs代谢失调提供了新的机制性见解.

关键词:

胃肠病学胃肠病学人类新陈代谢的人类新陈代谢.基因调节的分子机制

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