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DKK3通过增加MFF介导的线粒体功能障碍以Wnt/β-catenin通路依赖的方式促进纤维化

Jianling Song¹, Yanxia Chen¹, Yan Chen¹

¹Department of Nephrology, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi Province, P.R. China.

|April 29, 2024

概括

迪克科夫3 (DKK3) 通过增加m6A修饰,激活Wnt/β-catenin通路和增强MFF表达来促进纤维化,导致线粒体功能障碍和慢性病中的氧化应激.

科学领域:

腎臟病學 (nephrology) 是一種醫學專業.
分子生物学分子生物学
生物化学生物化学

背景情况:

慢性病 (CKD) 是一种进展性疾病,治疗选择有限.
纤维化 (RF) 是CKD的关键病理结果,导致功能障碍.
迪克科夫3 (DKK3) 在CKD病原体中的作用,特别是其潜在机制,仍然不完全理解.

研究的目的:

阐明Dickkopf 3 (DKK3) 在慢性病 (CKD) 中导致纤维化 (RF) 的分子机制.
调查涉及m6A修饰,Wnt/β-catenin信号传递和MFF表达在DKK3介导的RF中的调节途径.

主要方法:

利用过氧化 (H2O2) 处理的HK-2细胞和单边尿道阻塞 (UUO) 的小鼠模型来模拟RF.
使用各种生化和组织学技术评估功能,亡,氧化应激和线粒体功能.
采用了分子生物学方法,包括西方涂抹,qRT-PCR,免疫光和双光酶试验,以确定分子相互作用和表达水平.

主要成果:

在两种射频模型中,DKK3表达显著上调.
在UUO小鼠和HK-2细胞中,DKK3敲击改善了损伤,减少了氧化应激,并抑制了apoptosis和线粒体功能障碍.
从机制上来看,DKK3上调与METTL3介导的m6A修饰有关,该修饰激活了TCF4/β-catenin通路并增加了MFF转录.

结论:

DKK3,通过m6A修改进行上调,通过激活Wnt/β-catenin通路并增加MFF表达,促进RF进展.
这一级联导致线粒体功能障碍和氧化应激,突出显示DKK3作为CKD潜在的治疗点.

关键词:

DKK3 DKK3 DKK3 DKK3 DKK3 DKK3 DKK3 DKK3 DKK3 DKK3 多年财政框架的多年财政框架.患有脏纤维化 m6A 修改的修改线粒体的恒常状态是线粒体的恒常状态

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