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激活转录因子3通过抑制内源性反元素来缓解小鼠的急性肝损伤

Yu Liu¹, Yifan Niu², Xueting Shan¹

¹College of Animal Science and Technology & College of Veterinary Medicine, Zhejiang A&F University, Key Laboratory of Applied Technology on Green-Eco-Healthy Animal Husbandry of Zhejiang Province, Provincial Engineering Research Center for Animal Health Diagnostics & Advanced Technology, Hangzhou, Zhejiang 311300, China.

International journal of biological macromolecules

|November 22, 2025

概括

激活转录因子3 (ATF3) 通过抑制内源逆元素 (ERE) 来防止急性肝损伤. 这种新的机制降低了炎症,促进了肝脏的修复,提供了潜在的治疗点.

科学领域:

肝病学肝病学是一种肝病学.
分子生物学分子生物学
免疫学免疫学免疫学

背景情况:

激活转录因子3 (ATF3) 在慢性肝病中起着已知的作用,但其在急性肝损伤中的作用尚不清楚.
迫切需要有效的治疗急性肝损伤.

研究的目的:

研究ATF3在急性肝损伤中的保护作用.
阐明ATF3在这种条件下的功能背后的分子机制.

主要方法:

碳四化物 (CCl4) 诱导的急性肝损伤小鼠模型.
使用肝星细胞 (HSC) 的体外研究.

主要成果:

过度表达ATF3可缓解急性肝损伤症状,减少炎症并改善肝功能.
ATF3抑制了内源逆元素 (ERE) 激活,防止了基因组的不稳定性和cGAS/STING通路的激活.
ATF3通过结合它们的促进子区域直接抑制了ERE转录,抑制了促炎性细胞因子的产生 (例如,IFNβ).

结论:

在急性肝损伤中,ATF3充当RE激活的关键负调节剂.
ATF3可以缓解肝炎,并通过ERE调节促进肝脏的修复.
ATF3-ERE轴是急性肝损伤的潜在治疗标,并提供了对天生的免疫的转录因子调节的洞察.

关键词:

在ATF3中使用ATF3.急性肝损伤是什么意思内生逆元件内生逆元件炎症炎症是一种炎症.这是天生的免疫力.

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