Atherosclerosis remains the underlying process responsible for cardiovascular diseases and the high mortality rates associated. This chronic inflammatory disease progresses with the formation of occlusive atherosclerotic plaques over the inner walls of vascular vessels, with oxidative stress being an important element of this pathology. Oxidation of low-density lipoproteins (ox-LDL) induces endothelial dysfunction, foam cell activation, and inflammatory response, resulting in the formation of fatty streaks in the atherosclerotic wall. With this in mind, different approaches aim to reduce oxidative damage as a strategy to tackle the progression of atherosclerosis. Special attention has been paid in recent years to the transcription factor Nrf2 and its downstream-regulated protein heme oxygenase-1 (HO-1), both known to provide protection against atherosclerotic injury. In the current review, we summarize the involvement of oxidative stress in atherosclerosis, focusing on the role that these antioxidant molecules exert, as well as the potential therapeutic strategies applied to enhance their antioxidant and antiatherogenic properties.

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Nrf2 和 Heme Oxygenase-1 参与动脉粥样硬化相关的氧化应激

动脉粥样硬化仍然是导致心血管疾病和相关高死亡率的潜在过程。这种慢性炎性疾病随着血管内壁上的闭塞性动脉粥样硬化斑块的形成而发展，氧化应激是这种病理学的一个重要因素。低密度脂蛋白 (ox-LDL) 的氧化会导致内皮功能障碍、泡沫细胞活化和炎症反应，从而导致动脉粥样硬化壁中脂肪条纹的形成。考虑到这一点，不同的方法旨在减少氧化损伤，作为解决动脉粥样硬化进展的策略。近年来特别关注转录因子 Nrf2 及其下游调节蛋白血红素加氧酶-1 (HO-1)，两者都已知可提供针对动脉粥样硬化损伤的保护。在当前的综述中，我们总结了氧化应激在动脉粥样硬化中的参与，重点关注这些抗氧化分子发挥的作用，以及用于增强其抗氧化和抗动脉粥样硬化特性的潜在治疗策略。