Atherosclerosis. 2010 Sep;212(1):30-1. doi: 10.1016/j.atherosclerosis.2010.04.036. Epub 2010 May 6.
Fatty-acid-induced endoplasmic reticulum stress has been recently described as a novel mechanism involved in the genesis of atherosclerosis. Here we show that statins, a class of drug widely employed in the clinical management of hypercholesterolemia, reduces lipid-induced macrophage endoplasmic reticulum stress in an isolated cell system and in LDL receptor knockout mice. Given the importance of endoplasmic reticulum stress as an inducer of inflammation, we suspect that the novel mechanism of action herein described for statins may play a major role on its beneficial effects in the prevention of cardiovascular disease.
脂肪酸诱导的内质网应激最近被描述为参与动脉粥样硬化形成的一种新机制。在这里，我们表明他汀类药物，一类广泛用于临床高胆固醇血症治疗的药物，可降低分离细胞系统和 LDL 受体敲除小鼠中脂质诱导的巨噬细胞内质网应激。鉴于内质网应激作为炎症诱导剂的重要性，我们推测本文所述的他汀类药物的新作用机制可能在其预防心血管疾病的有益作用中发挥主要作用。
