Cardiovascular disease (CVD) is the number one cause of death in the United States and worldwide. The most common cause of cardiovascular disease is atherosclerosis, or formation of fatty plaques in the arteries. Low-density lipoprotein (LDL), termed "bad cholesterol", is a large molecule comprised of many proteins as well as lipids including cholesterol, phospholipids, and triglycerides. Circulating levels of LDL are directly associated with atherosclerosis disease severity. Once thought to simply be caused by passive retention of LDL in the vasculature, atherosclerosis studies over the past 40-50 years have uncovered a much more complex mechanism. It has now become well established that within the vasculature, LDL can undergo many different types of oxidative modifications such as esterification and lipid peroxidation. The resulting oxidized LDL (oxLDL) has been found to have antigenic potential and contribute heavily to atherosclerosis associated inflammation, activating both innate and adaptive immunity. This review discusses the many proposed mechanisms by which oxidized LDL modulates inflammatory responses and how this might modulate atherosclerosis.

中文翻译：

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氧化的低密度脂蛋白如何激活炎症反应。

心血管疾病（CVD）是美国和全球范围内的第一大死因。心血管疾病的最常见原因是动脉粥样硬化或动脉中脂肪斑的形成。低密度脂蛋白（LDL），称为“坏胆固醇”，是一个由许多蛋白质以及包括胆固醇，磷脂和甘油三酸酯在内的脂质组成的大分子。LDL的循环水平与动脉粥样硬化疾病的严重程度直接相关。人们曾经认为，LDL仅是由于LDL在血管中的被动滞留所致，但过去40至50年间的动脉粥样硬化研究发现了更为复杂的机制。现在已经众所周知，在脉管系统中，LDL可以经历许多不同类型的氧化修饰，例如酯化和脂质过氧化。已发现所得的氧化的LDL（oxLDL）具有抗原性，并在与动脉粥样硬化相关的炎症中起重要作用，从而激活先天免疫和适应性免疫。这篇综述讨论了氧化LDL调节炎症反应的许多提议机制，以及这可能如何调节动脉粥样硬化。