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VEGFB通过抑制巨细胞中北上腺素清除来促进脂肪组织热生成

Lei Wang¹, Jing Jin², Nuo Zhang²

¹Department of Pathophysiology, Key Laboratory of Targeted Intervention of Cardiovascular Disease and Molecular Intervention, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, China; Department of Pathology, Affiliated BenQ Hospital of Nanjing Medical University, Nanjing, China.

Biochimica et biophysica acta. Molecular basis of disease

|October 8, 2024

概括

血管内皮生长因子B (VEGFB) 和其受体VEGFR1通过调节巨细胞信号来增强白脂肪组织 (WAT) 热生成. 这种VEGFB/VEGFR1通路对于WAT色和适应性热量产生至关重要.

科学领域:

代谢和内分泌学
细胞生物学细胞生物学
脂肪组织生物学脂肪组织生物学

背景情况:

阿迪波基因对色脂肪细胞的适应性热生成至关重要.
控制热生成的精确调节机制仍然不完全理解.
白色脂肪组织 (WAT) 在能量平衡中起着重要作用.

研究的目的:

研究血管内皮生长因子B (VEGFB) 和其受体VEGFR1在白脂肪组织 (WAT) 热生成中的作用.
阐明参与VEGFB/VEGFR1-介导热生成的信号通路.
为了确定这个信号电路对WAT色的贡献.

主要方法:

使用小鼠模型,对脂细胞VEGFB.进行向性切除和补充.
研究了巨细胞VEGFR1淘汰对WAT热生成的影响.
进行了涉及p38基因激活蛋白激酶 (MAPK) 信号和北上腺素清除途径的机制研究.

主要成果:

热生成激活在小鼠皮下WAT (scWAT) 上调节脂肪细胞中的VEGFB和巨细胞中的VEGFR1.
脂肪细胞VEGFB缺乏会影响WAT色,而VEGFB补充会促进热生成.
巨细胞VEGFR1对于VEGFB的热能效应至关重要,通过抑制p38 MAPK信号传递和北上腺素清除而起作用.

结论:

VEGFB/VEGFR1信号通路是白色脂肪组织中热生成的关键调节器.
这一途径调节巨细胞功能,以增强北上腺素介导的热量产生.
与能量消耗相关的代谢障碍的VEGFB/VEGFR1信号是一个潜在的治疗目标.

关键词:

脂肪组织的脂肪组织.巨细胞是一个巨细胞.热生成是一种热生成.血管内皮生长因子B (VEGFB)血管内皮生长因子受体1 (VEGFR1)

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