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低剂量辐射通过激活cGAS信号通路来促进高脂肪饮食诱导的动脉样硬化

Xiaochang Liu¹, Xin Huang¹, Jinhua Luo²

¹Department of Radiation Biology, Beijing Key Laboratory for Radiobiology, Beijing Institute of Radiation Medicine, Beijing 100850, China.

Biochimica et biophysica acta. Molecular basis of disease

|July 27, 2024

概括

低剂量辐射 (LDR) 结合高脂肪饮食 (HFD) 加快了小鼠的动脉样硬化发展. 这种协同效应涉及通过cGAS-STING通路的脂质代谢变化和炎症,为心血管疾病风险提供了新的见解.

科学领域:

心血管研究研究心血管研究
环境健康环境健康
分子生物学分子生物学

背景情况:

动脉样硬化 (AS) 是一种主要的心血管疾病,具有重大健康和经济负担.
众所周知,高脂肪饮食 (HFD) 可能会恶化AS,而低剂量辐射 (LDR) 是一个环境因素,其影响尚不清楚.
HFD和LDR对AS发展的综合影响需要进一步研究.

研究的目的:

研究HFD和LDR对ApoE-/-小鼠动脉样硬化发展的联合影响.
阐明潜在的机制,包括脂质代谢和炎症信号通路.

主要方法:

动脉硬化模型使用暴露于HFD和不同剂量的LDR (0.1或0.2 Gy) 的ApoE-/-小鼠.
使用多普勒超声波,H&E染色和油红O染色对血管病变的评估.
通过西式涂抹,免疫组织化学 (IHC) 和非向性脂管学 (LC-MS) 分析分子变化.

主要成果:

长期的LDR暴露 (0.2 Gy) 在ApoE-/-小鼠中显著增加了血管硬和大动脉病变.
观察到HFD和LDR的协同效应,与脂质代谢失调和炎症信号相关.
通过增加线粒体DNA和cGAS蛋白,LDR激活了cGAS-STING通路,导致IFN-α/β释放和放大炎症.

结论:

这项研究揭示了LDR在动脉样硬化中的作用的新见解,强调了与HFD的协同效应.
cGAS-STING信号通路与LDR和HFD诱导的动脉样硬化的联合发病有关.
这些发现强调了与环境和饮食因素结合相关的潜在心血管风险.

关键词:

动脉样硬化是一种动脉样硬化.cGAS-STING 的使用情况.有高脂肪的饮食.低剂量辐射的辐射剂量很低.

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