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棕酸通过PKM2的棕化加速内皮细胞损伤和心血管功能障碍

Yu He¹, Senlin Li^2,3,4, Lujing Jiang¹

¹Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, National and Local United Engineering Lab of Druggability and New Drugs Evaluation, Guangdong Engineering Laboratory of Druggability and New Drug Evaluation, Guangdong Provincial Key Laboratory of New Drug Design and Evaluation, Sun Yat-sen University, Guangzhou, 510006, P. R. China.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

|December 12, 2024

概括

高水平的棕酸与心血管风险有关. 在Cys31中PKM2蛋白的棕化驱动这种损伤,通过损害内皮糖解,导致心血管功能障碍.

科学领域:

心血管生物学心血管生物学
分子医学是分子医学.
生物化学生化学

背景情况:

高血清棕酸 (PA) 与心血管疾病的发病有关.
蛋白棕化在PA引起的心血管功能障碍中的作用尚不清楚.

研究的目的:

为了研究蛋白质棕化对PA诱导的心血管功能障碍的参与.
为了确定特定的蛋白质和机制,这种过程的基础.

主要方法:

临床队列研究 (1040名患者) 和ApoE-/-小鼠模型.
在体外内皮细胞实验中使用棕化抑制剂/促进剂.
棕基蛋白质组学分析,位点定向突变发生 (PKM2-C31S) 和内皮特异性基因传递 (AAV-C31S PKM2endo).

主要成果:

高血压与主要不良心血管事件 (MACE) 和患者死亡有关.
在小鼠中,PA治疗导致血压升高,心脏和内皮功能受损,并促进动脉样硬化.
抑制棕化保护了PA诱导的内皮损伤,而促进则加剧了损伤.
在Cys31的PKM2棕化被确定为一个关键的调解剂,损害PKM2四重化,抑制pyruvate kinase活性,并减少内皮糖解.
鉴定出zDHHC13是负责PKM2.2的棕酸转移酶.

结论:

PKM2-C31棕化是PA诱导的内皮损伤和心血管功能障碍的一个关键机制.
向PKM2棕化可能为与高棕酸水平相关的心血管疾病提供治疗策略.

关键词:

在PKM2中,PKM2是PKM2.心血管功能障碍 - 心血管功能障碍脑内皮损伤的损伤棕酸是一种棕酸.棕细胞代谢 (palmitoylation) 是一种

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