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痕信号通过线粒体通路调节小鼠周周血管脂肪组织功能

Chenhao Yang^1,2, Xuehui Yang¹, Anne Harrington¹

¹Center for Molecular Medicine, MaineHealth Institute for Research, Scarborough, ME 04074, USA.

|October 28, 2023

概括

周周血管脂肪组织 (PVAT) 中的痕信号损害了线粒体功能,并促进了铁亡,导致血管反应能力发生改变. 这项研究揭示了PVAT功能障碍如何影响血管健康.

科学领域:

血管生物学血管生物学
脂肪组织生物学脂肪组织生物学
细胞的新陈代谢

背景情况:

周血管脂肪组织 (PVAT) 通过分泌的因素影响血管功能.
肥胖会激活PVAT中的Notch信号,导致脂肪细胞白化和热能特性丧失.
在PVAT中构成性口激活模仿了与肥胖相关的变化.

研究的目的:

调查受PVAT中Notch信号影响的下游分子通路.
阐明诺奇诱导的PVAT功能障碍对线粒体功能和铁亡的影响.
确定PVAT中激活的Notch信号对血管反应的后果.

主要方法:

从对照和Notch激活小鼠 (N1ICD;Adipoq-Cre) 中对PVAT进行蛋白质组分析.
评估PVAT衍生型流体血管分离细胞中的线粒体呼吸和脂肪生成.
导线肌图用于评估来自实验小鼠的大动脉中的血管活性.

主要成果:

在PVAT中口激活改变了与代谢,脂肪细胞平衡,线粒体功能和铁亡有关的蛋白质特征.
激活的Notch信号降低了PVAT细胞中的线粒体呼吸,而不会影响脂肪生成或线粒体数量.
口激活促进了PVAT脂肪细胞中的脂质过氧化和铁,导致血管收缩增加和大动脉血管松减少.

结论:

在脂肪组织中增加的Notch信号驱动PVAT白化,线粒体功能障碍和铁亡.
这些PVAT变化导致血管保护信号受损和血管活性改变.
这项研究强调了脂肪细胞Notch信号传递,线粒体动力学和血管生理学之间的新联系.

关键词:

口信号传输是没有的.线粒体的动力学周围的周周脂肪组织组织.

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