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持续的低压性缺氧可能会促进阿波利波蛋白E缺乏小鼠的动脉样硬化进展

Shouming Luo¹, Xiaogen Ma¹, Weiqiang Wu¹

¹Department of Cardiovascular Medicine, Center for Circadian Metabolism and Cardiovascular Disease, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China.

International journal of medical sciences

|June 16, 2023

概括

持续的低血压缺氧 (CHH) 通过增加斑块生长,炎症和血管生成来加速小鼠的动脉样硬化. 这种高海拔模拟会使动脉样硬化斑块的稳定性和病变大小恶化.

科学领域:

心血管研究研究心血管研究
环境生理学环境生理学
动脉样硬化研究动脉样硬化研究

背景情况:

众所周知,间歇性normobaric缺氧可以促进动脉样硬化斑块的进展.
持续性低压性缺氧 (CHH) 对动脉样硬化的影响,这种持续性低压性缺氧 (CHH) 是高海拔环境的特征,对动脉样硬化的影响仍未得到充分研究.

研究的目的:

调查持续性低血压缺氧 (CHH) 对动脉样硬化的发展和稳定性的影响.
确定血管新生和炎症在CHH诱导的动脉样硬化进展中的作用.

主要方法:

在高胆固醇饮食中的ApoE-/-小鼠被暴露在CHH (10%氧,364 mmHg) 中4周.
评估了动脉样硬化病变的大小,斑块稳定性,斑块内血管生成 (CD31,内素) 和炎症标志物.
使用定量实时PCR (qRT-PCR) 和免疫组织化学分析分子变化.

主要成果:

CHH显著促进了动脉样硬化病变的生长,并降低了斑块稳定性 (p=0.0017).
CHH暴露导致光滑肌细胞和原减少,但斑块内的巨细胞和脂质增加 (p<0.001).
增加的CD31和内素表达表明增强的内血管生成,与更高的单细胞化疗蛋白-1和矩阵金属蛋白酶-2水平相关.

结论:

持续的低血压缺氧 (CHH) 在ApoE-/-小鼠中加速动脉样硬化进展.
通过增强内血管生成和炎症,CHH促进动脉样硬化.
研究结果强调了高海拔模拟环境对心血管健康的有害影响.

关键词:

高度的高度高度的高度.血管新生是因为血管新生.动脉样硬化动脉样硬化催眠症催眠症的催眠症是什么这是一种炎症炎症炎症炎症.斑块的不稳定性不稳定性

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