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纤维素酸和Malondialdehyde-Acetaldehyde-modified纤维素激活巨细胞并促进冠状动脉内皮细胞炎症

Wenxian Zhou¹, Hannah J Johnson¹, Michael J Duryee^1,2

¹Department of Internal Medicine, Division of Rheumatology, University of Nebraska Medical Center, Omaha, NE 68198, USA.

Current issues in molecular biology

|November 26, 2025

概括

风湿性关节炎 (RA) 患者心力衰竭 (HF) 显示由于修饰纤维素原 (FIB-MAA-CIT) 的心脏炎症增加. 这种蛋白质修饰促进了巨细胞和内皮细胞之间的交叉交流,推动了RA中的HF进展.

科学领域:

心血管研究研究心血管研究
免疫学免疫学免疫学
类风湿病学类风湿病学

背景情况:

类风湿性关节炎 (RA) 与较高的心血管死亡率有关,特别是心力衰竭 (HF).
转化后的修改,如素化 (CIT) 和甲-乙 (MAA) 添加,都涉及到RA,但它们在RA相关的HF中的作用尚不清楚.
了解这些修改对心脏的影响对于RA-HF患者的治疗结果至关重要.

研究的目的:

调查RA-HF患者心脏组织中MAA和CIT添加物的存在.
探索MAA和CIT在纤维素原上 (FIB-MAA-CIT) 调节巨细胞和内皮细胞之间交叉的机制.
确定潜在的治疗目标,以缓解RA中的HF.

主要方法:

对RA-HF患者和非RA HF对照患者的心脏组织分析MAA和CIT添加物和原沉积.
在体外研究中,使用人类冠状动脉内皮细胞 (HCAEC) 和用未经修改的纤维素素 (FIB) 刺激的巨细胞与FIB-MAA-CIT.
对炎症标志物表达 (MCP-1,IL-6,ICAM-1,VCAM-1) 和信号通路 (NF-κB,p38) 的评估.

主要成果:

在RA-HF患者的心脏中观察到MAA和CIT adducts的升高,以及血管周MAA-CIT同局部和原沉积.
在HCAEC中,FIB-MAA-CIT诱导了炎症反应,由受刺激的巨细胞的介质放大.
由FIB-MAA-CIT引起的巨细胞激活涉及NF-κB和p38通路,并抑制这些减少的细胞因子分泌和随后的内皮细胞反应.

结论:

修改后的蛋白质,特别是FIB-MAA-CIT,通过RA-HF的巨细胞-内皮细胞交叉促进心肌炎症.
这种交叉交互是由巨细胞中的NF-κB和p38信号通路介导的.
针对这些翻译后修改提供了一个潜在的治疗策略,用于管理类风湿性关节炎中心力衰竭.

关键词:

氨酸 (Citrulline) 是一种氨酸.细胞内皮细胞的内皮细胞.心脏衰竭是因为心脏衰竭.马隆迪甲乙甲翻译后的修改翻译后的修改类风湿性关节炎类风湿性关节炎

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