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通过调节CLCF1/STAT3信号通路,MAFF可以缓解肝缺血再输血损伤

Dengliang Lei¹, Yihua Wang², Shanshan Li¹

¹Department of Hepatobiliary Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.

Cellular & molecular biology letters

|April 1, 2025

概括

MAFF通过减少细胞死亡和炎症来保护肝脏免受缺血-再输液损伤. 这种转录因子激活了CLCF1/STAT3通路,为肝脏治疗提供了潜在的治疗策略.

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:

肝脏缺血-再输损伤 (IRI) 是肝脏手术和移植期间的常见并发症.
肝脏IRI背后的分子机制尚未完全理解.
在肝脏IRI之后,v-maf肌肉aponeurotic纤维瘤瘤原基因同类F (MAFF) 表达上调.

研究的目的:

调查MAFF在肝脏IRI中的作用.
探索MAFF在肝脏保护方面的治疗潜力.

主要方法:

使用腺病毒载体来操纵小鼠的MAFF表达.
使用了高通量测序和CUT&Tag/RNA测序.
对肝细胞亡和前炎性细胞因子表达的分析.

主要成果:

在缺血-再输血之后,MAFF的表达得到了上调.
减少MAFF表达会加剧肝损伤和炎症.
过度表达MAFF可以改善肝脏IRI.
通过BACH1异构体,MAFF直接针对CLCF1,激活STAT3信号.

结论:

通过减少肝细胞亡和炎症,MAFF可以缓解肝脏IRI.
MAFF的保护作用通过CLCF1/STAT3信号通路进行介导.
MAFF 代表了一种潜在的肝脏保护治疗点.

关键词:

在BACH1的基础上.在CLCF1中,肝脏缺血再输血马夫 (MAFF) 是一个在STAT3中,我们可以使用STAT3.

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