Offermann M K, Medford R M
Department of Medicine, Emory University School of Medicine, Atlanta, Georgia 30322.
Heart Dis Stroke. 1994 Jan-Feb;3(1):52-7.
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.
当前的动脉粥样硬化发生模型将血管壁氧化状态异常与免疫系统相互作用联系起来，导致局部炎症和生长反应的循环，从而形成成熟动脉粥样硬化病变的特征。低密度脂蛋白（LDL）的氧化修饰可能是这一过程的重要表现和介质，尽管其对动脉粥样硬化发生的贡献程度尚未得到直接评估。另一个重要机制可能涉及血管内皮细胞的氧化状态通过特定转录调节因子与控制参与该疾病过程的基因表达之间的联系。这进一步拓展了氧化应激作为动脉粥样硬化发病机制中重要调节信号的概念，并为开发新型治疗方案、药物设计以及疾病状态的诊断评估提供了重要范例。
