抗氧化剂与动脉粥样硬化:分子视角。

M K Offermann, R M Medford
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引用次数: 0

摘要

目前的动脉粥样硬化模型将血管壁氧化状态的异常与免疫系统的相互作用联系起来,导致局部炎症和生长反应的循环,从而导致成熟动脉粥样硬化病变的特征。低密度脂蛋白的氧化修饰可能是这一过程的重要表现和中介,尽管其对动脉粥样硬化的影响程度尚未得到直接评估。另一个重要的机制可能涉及血管内皮细胞的氧化状态的联系,通过特定的转录调节因子,来控制参与该疾病过程的基因的表达。这进一步扩展了氧化应激在动脉粥样硬化发病机制中的重要调控信号的观点,并为开发新的治疗方案、药物设计和疾病状态的诊断评估提供了重要的范式。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Antioxidants and atherosclerosis: a molecular perspective.

Current models of atherogenesis link abnormalities in the oxidative state of the vascular wall with interactions with the immune system, leading to a cycle of localized inflammatory and growth responses that result in the characteristics of the mature atherosclerotic lesion. The oxidative modification of LDL may be an important manifestation and mediator of this process, although the degree to which this contributes to atherogenesis has not been directly assessed. Another important mechanism may involve the linkage of the oxidative state of the vascular endothelial cell, through specific transcriptional regulatory factors, to control the expression of a gene involved in this disease process. This further expands the idea of oxidative stress as an important regulatory signal in the pathogenesis of atherosclerosis and provides important paradigms for the development of novel therapeutic treatment regimens, drug design, and diagnostic assessments of disease state.

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