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PFKFB3的m6A依赖性上调驱动在死角性肠球炎中的巨介导炎症

Chaoting Lan^1,2,3, Bowen Tian⁴, Yingyan Liu¹

¹Center for Medical Research on Innovation and Translation, Guangzhou First People's Hospital, the Second Affiliated Hospital of South China University of Technology, Guangzhou, Guangdong, China.

Antioxidants & redox signaling

|November 15, 2025

概括

在死性肠球炎 (NEC) 中,减少PFKFB3mRNA的N6-甲基氨酸 (m6A) 甲基化促进炎症. 用药物向PFKFB3,通过减少炎症和组织损伤,为NEC提供了一个新的治疗策略.

科学领域:

表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.
代谢途径代谢途径
炎症性疾病是一种炎症性疾病.

背景情况:

死性肠球炎 (NEC) 是新生儿严重的胃肠道疾病.
表观遗传修饰的作用,特别是N6-甲基氨酸 (m6A) 甲基化,在NEC病原发生过程中尚未完全理解.
6-果糖-2-激酶/果糖-2,6-双酸酶-3 (PFKFB3) 是糖分解的一个关键调节剂.

研究的目的:

研究m6A甲基化在NEC中调节PFKFB3表达中的作用.
探索在NEC中准PFKFB3的治疗潜力.

主要方法:

在人类NEC组织中分析m6A甲基化.
在体内和体外的NEC模型 (脂多糖-低氧-感冒压力,THP-1-分化巨细胞).
评估PFKFB3的表达,糖溶性流量,反应性氧物种 (ROS) 的产生,以及巨细胞的两极分化.
药理上抑制PFKFB3.3. 药理上抑制PFKFB3.

主要成果:

在人类NEC组织中观察到PFKFB3mRNA的m6A甲基化减少,导致PFKFB3稳定性和蛋白质水平增加.
PFKFB3驱动的糖解通过ROS积累促进了M1巨分化,在NEC模型中加剧了肠道炎症.
在NEC模型中,对PFKFB3的药理抑制显著降低了ROS,巨细胞透和粘膜损伤.

结论:

一个代谢-表观遗传轴涉及PFKFB3mRNA的减少m6A甲基化,有助于NEC的病原性.
抑制PFKFB3代表了一种有前途的治疗策略,用于减轻NEC的炎症和组织损伤.
这项研究提供了NEC中m6A介导机制的第一个证据,并突出了PFKFB3作为一种新的治疗点.

关键词:

这是一种N6-甲基氨酸.PFKFB3B3 是一个很好的选择.巨细胞是一个巨细胞.代谢异常代谢异常死性肠球炎 (necrotizing enterocolitis) 是一种致死性肠球炎的疾病.

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