Hedrick C C, Kim M D, Natarajan R D, Nadler J L
Division of Cardiology, University of California Los Angeles 90095, USA.
Adv Exp Med Biol. 1999;469:455-60. doi: 10.1007/978-1-4615-4793-8_67.
In summary, we suggest that hyperglycemia causes upregulation of 12-lipoxygenase activity. The increased production of 12-LO products, 12(S) and 15(S)-HETE, activates monocyte integrins which result in enhanced adhesion of monocytes to endothelium. The binding of monocytes to endothelium is a key early event in development of atherosclerosis. Upregulation of this process by vascular cells exposed to chronic elevations in glucose may be one explanation for the accelerated atherosclerosis observed in patients with Type 2 diabetes.
总之，我们认为高血糖会导致12-脂氧合酶活性上调。12-脂氧合酶产物12(S)和15(S)-羟基二十碳四烯酸（HETE）产量的增加会激活单核细胞整合素，从而增强单核细胞与内皮的黏附。单核细胞与内皮的结合是动脉粥样硬化发展过程中的一个关键早期事件。暴露于长期高血糖环境的血管细胞对这一过程的上调可能是2型糖尿病患者动脉粥样硬化加速的一种解释。
