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在THP-1巨细胞中,LPS通过HKDC1调解了cuproptosis和炎症

Langlin Ou¹, Zitong Meng¹, Jian Mei¹

¹College of Medical Laboratory Science and Technology, Harbin Medical University, Daqing 163319, China.

Acta biochimica et biophysica Sinica

|July 22, 2025

概括

脂聚糖 (LPS) 降低了铜驱动的细胞死亡 - - cuproptosis,并通过增加宏细胞中含有1 (HKDC1) 酶域的表达增加炎症. 抑制HKDC1激活了cuproptosis并减少了炎症,提供了一个新的抗炎症策略.

科学领域:

细胞生物学细胞生物学
免疫学免疫学免疫学
生物化学生物化学

背景情况:

质亡是一种依赖铜的细胞死亡途径,与炎症有关.
含有1 (HKDC1) 的六金酶域调节了线粒体功能,但其在亡和炎症中的作用尚不清楚.

研究的目的:

调查HKDC1在巨细胞中脂聚糖 (LPS) 诱导的炎症和亡中的作用.
阐明LPS影响HKDC1表达和cuproptosis的分子机制.

主要方法:

巨细胞活力和细胞化试验 (CCK8).
西方斑块和RT-qPCR用于炎症因素和cuproptosis蛋白质.
对于HKDC1的表达和定位,ChIP-qPCR和免疫光.
在体内败血症模型.

主要成果:

通过激活糖解和通过TLR4通过HKDC1上调调节,LPS增加了炎症因子,并减少了巨细胞中的cuproptosis.
HKDC1 knockdown 抑制了葡萄糖分解,诱导了亡,并且涉及YY1 与HKDC1促进体结合.
HKDC1与HSCB和FDX1相互作用,增加细胞内铜和cuproptosis.
在体内减轻了HKDC1的败血症.

结论:

通过HKDC1介导的途径,LPS减轻了cuproptosis,并促进了炎症.
HKDC1是LPS诱导的炎症和cuproptosis的一个关键调节器.
准HKDC1提供了一个潜在的依赖cuproptosis的抗炎策略.

关键词:

一个HKDC1是HKDC1.在LPS中使用LPS.这就是cuproptosis.葡萄糖溶解是什么这是一种炎症炎症炎症炎症.

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