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通过向KEAP1/NRF2相互作用来抑制巨细胞铁亡,MCL可以减轻动脉样硬化

Xing Luo¹, Yuehong Wang², Xinxin Zhu¹

¹Department of Cardiology, 2nd Affiliated Hospital of Harbin Medical University, Harbin, 150001, PR China; National Key Laboratory of Frigid Zone Cardiovascular Diseases; The Key Laboratory of Myocardial Ischemia, Chinese Ministry of Education, Harbin 150001, PR China.

|December 15, 2023

概括

米歇利化物 (MCL) 通过抑制巨细胞铁死来降低动脉样硬化. 它通过与KEAP1竞争结合来激活NRF2通路,为动脉样硬化提供了潜在的治疗策略.

科学领域:

心血管研究研究心血管研究
分子医学是分子医学.
免疫学免疫学免疫学

背景情况:

米歇利奥利德 (MCL) 是帕瑟诺利德的一种代谢物,显示出临床潜力.
动脉样硬化中MCL的确切机制在很大程度上是未知的.

研究的目的:

为了研究MCL对动脉样硬化的影响.
阐明MCL作用的潜在分子机制.

主要方法:

接受高脂肪饮食的ApoE-/-小鼠接受了MCL治疗.
分析包括斑块面积,脂质沉积和原含量.
在体外研究中使用了用MCL和ox-LDL治疗的巨细胞来评估铁亡,NRF2激活,线粒体功能和氧化应激.

主要成果:

治疗MCL显著降低了动脉硬性斑块的进展,减少了斑块面积和脂质沉积,同时增加了原蛋白含量.
MCL增加了巨细胞中的GPX4和xCT水平,改善了线粒体功能,减少了氧化应激,并抑制了脂质过氧化.
通过抑制KEAP1/NRF2复合体的形成,MCL激活了NRF2通路,这对其抗费洛灭作用至关重要.

结论:

通过NRF2通路激活,MCL通过抑制巨细胞铁死来抑制动脉样硬化.
MCL在竞争中与KEAP1的Arg483位点结合,这是其治疗效果的关键机制.

关键词:

动脉样硬化是一种动脉样硬化.铁化是铁化的一种.KEAP1/NRF2 的使用情况.在 MCL 和 MCL 之间.氧化应激是一种氧化应激.

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