Nicholls Stephen J, Hazen Stanley L
Departments of Cell Biology and Cardiovascular Medicine, Center for Cardiovascular Diagnostics and Prevention, Cleveland Clinic, Cleveland, OH, USA.
J Lipid Res. 2009 Apr;50 Suppl(Suppl):S346-51. doi: 10.1194/jlr.R800086-JLR200. Epub 2008 Dec 16.
Numerous lines of evidence implicate a role for myeloperoxidase (MPO) in the pathogenesis of atherosclerosis. Enriched within vulnerable plaque, MPO serves as an enzymatic source of eicosanoids and bioactive lipids and generates atherogenic forms of both low- and high-density lipoproteins. These factors likely contribute to clinical studies demonstrating that increased systemic levels of MPO and its oxidation products predict increased cardiovascular risk. As a result, interest has focused on the potential to target MPO for the development of new risk markers, imaging, and therapies to prevent cardiovascular events.
大量证据表明髓过氧化物酶(MPO)在动脉粥样硬化发病机制中起作用。MPO在易损斑块中含量丰富,是类花生酸和生物活性脂质的酶源,可生成低密度脂蛋白和高密度脂蛋白的致动脉粥样硬化形式。这些因素可能有助于临床研究表明,MPO及其氧化产物的全身水平升高预示着心血管风险增加。因此,人们的兴趣集中在靶向MPO以开发新的风险标志物、成像技术和预防心血管事件的疗法的潜力上。