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高胆固醇血引起的动脉样硬化的机制

Kailash Prasad¹, Manish Mishra²

¹Department of Physiology (APP), College of Medicine, University of Saskatchewan, Saskatoon, SK S7N 5A2, Canada.

Reviews in cardiovascular medicine

|July 30, 2024

概括

高胆固醇 (高胆固醇血症) 通过增加有害分子和炎症驱动动动脉硬化. 这导致冠状动脉疾病和中风等疾病.

科学领域:

心血管生物学心血管生物学
分子医学是分子医学.
病理生理学病理生理学

背景情况:

高胆固醇血症是动脉样硬化,冠状动脉疾病,中风和外周血管疾病的关键危险因素.
了解将高胆固醇与动脉样硬化联系在一起的机制对于开发有效的治疗方法至关重要.

研究的目的:

阐明高胆固醇血症促进动脉样硬化发展的详细机制.
确定关键的有机体生物分子和参与这个过程的途径.

主要方法:

对高胆固醇血症和动脉样硬化的现有文献的综述.
分析反应性氧物种 (ROS),炎症性细胞因子,粘附分子,生长因子和核因子-kappa-B (NF-κB) 的作用.
对AGE (RAGE) 轴和C反应蛋白 (CRP) 的高级糖化最终产品 (AGE) 受体参与的检查.

主要成果:

高胆固醇血症增加了许多异位原生物分子的产生,包括ROS,促炎细胞因子 (例如IL-1,TNF-α) 和粘附分子 (例如ICAM-1,VCAM-1).
它促进低密度脂蛋白-胆固醇 (LDL-C) 的氧化,并激活NF-κB.
高胆固醇血与AGE,氧化应激 (AGE/sRAGE比率) 和CRP的增加有关,以及AGE (sRAGE) 溶性受体的减少.

结论:

高胆固醇血症通过对神经动脉产生生物分子的上调调节诱导动脉样硬化.
AGE-RAGE轴和CRP在高胆固醇血驱动动的动脉样硬化中起着重要的作用.
针对这些途径可能为预防或治疗动脉样硬化提供治疗策略.

关键词:

在C-反应性蛋白质中.先进的糖化最终产品.其他原生生物分子.动脉样硬化动脉样硬化细胞粘附分子的细胞粘附分子细胞因子细胞因子超高胆固醇血症是一种高胆固醇血症.核因子-卡帕 B B 核因子有活性氧物种的反应性氧物种.

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