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内皮CD36调解了饮食诱导的大动脉硬度的增加

Javad Habibi¹, Vincent G DeMarco¹, Dongqing Chen¹

¹Department of Medicine-Endocrinology and Metabolism, University of Missouri School of Medicine, Columbia, MO 65212, USA; Harry S Truman Memorial Veterans Hospital, Research Service, 800 Hospital Dr, Columbia, MO 65201, USA.

Journal of molecular and cellular cardiology

|June 18, 2025

概括

西方饮食通过增加内皮细胞中的CD36促进动脉硬化,导致胰岛素抵抗和血管损伤. 移除这种CD36可以防止饮食引起的大动脉硬化和相关问题.

科学领域:

心血管生物学心血管生物学
代谢疾病代谢疾病
分子医学是分子医学.

背景情况:

西方饮食 (WD) 与肥胖,胰岛素抵抗和动脉硬化有关,这是主要的心血管疾病风险因素.
增加的CD36表达与子宫外脂质积累,胰岛素抵抗和动脉硬化相关.
内皮细胞特异性CD36 (ECCD36) 在WD引起的血管功能障碍中的作用尚不清楚.

研究的目的:

研究内皮细胞特异性CD36 (ECCD36) 在西方饮食诱导的大动脉胰岛素抵抗,脂质积累,炎症,纤维化,重塑和硬化中的作用.

主要方法:

雌性ECCD36淘汰赛和野生型小鼠被食WD或标准食16周.
动脉硬度通过脉冲波速度评估;血管功能通过线路肌图.
用分子和组织学技术分析基因表达,脂质含量和大动脉重塑.

主要成果:

WD诱导大动脉硬化,胰岛素耐药性和胰岛素信号受损 (PI3K/Akt通路).
与WD相关的变化包括mTOR/S6K激活,脂质失调,减少奥克卢丁,炎症和重塑.
这些WD诱导的异常在ECCD36淘汰赛小鼠中显著减弱.

结论:

在WD下增加ECCD36信号,有助于大动脉胰岛素抵抗,脂质积累和内皮功能障碍.
在应对西方饮食时,ECCD36促进炎症,纤维化,血管重塑和动脉硬化.
向ECCD36可能提供一种治疗策略,用于预防饮食引起的心血管并发症.

关键词:

动脉的硬性动脉的硬性 CD36 CD36 CD36 CD36 CD36 CD36 CD36 CD36 CD36 CD36 CD36 CD36 CD36 CD36 内皮细胞是内皮细胞.胰岛素耐药性胰岛素耐药性是一种肥胖问题肥胖问题

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