Department of Adult Cardiology, Deutsches Herzzentrum München, Technische Universität, Lazarettstrasse 36, 80636 Munich, Germany.
Clin Chim Acta. 2019 Jun;493:36-51. doi: 10.1016/j.cca.2019.02.022. Epub 2019 Feb 21.
Myeloperoxidase (MPO) is a member of the superfamily of heme peroxidases that is mainly expressed in neutrophils and monocytes. MPO-derived reactive species play a key role in neutrophil antimicrobial activity and human defense against various pathogens primarily by participating in phagocytosis. Elevated MPO levels in circulation are associated with inflammation and increased oxidative stress. Multiple lines of evidence suggest an association between MPO and cardiovascular disease (CVD) including coronary artery disease, congestive heart failure, arterial hypertension, pulmonary arterial hypertension, peripheral arterial disease, myocardial ischemia/reperfusion-related injury, stroke, cardiac arrhythmia and venous thrombosis. Elevated MPO levels are associated with a poor prognosis including increased risk for overall and CVD-related mortality. Elevated MPO may signify an increased risk for CVD for at least 2 reasons. First, low-grade inflammation and increased oxidative stress coexist with many metabolic abnormalities and comorbidities and consequently an elevated MPO level may represent an increased cardiometabolic risk in general. Second, MPO produces a large number of highly reactive species which can attack, destroy or modify the function of every known cellular component. The most common MPO actions relevant to CVD are generation of dysfunctional lipoproteins with an increased atherogenicity potential, reduced NO availability, endothelial dysfunction, impaired vasoreactivity and atherosclerotic plaque instability. These actions strongly suggest that MPO is directly involved in the pathophysiology of CVD. In this regard MPO may be seen as a mediator or an instrument through which inflammation promotes CVD at molecular and cellular level. Clinical value of MPO therapeutic inhibition remains to be tested.
髓过氧化物酶（MPO）是血红素过氧化物酶超家族的成员，主要在中性粒细胞和单核细胞中表达。MPO 衍生的活性物质通过参与吞噬作用，在中性粒细胞的抗菌活性和人体防御各种病原体中发挥关键作用。循环中 MPO 水平升高与炎症和氧化应激增加有关。多条证据表明 MPO 与心血管疾病（CVD）之间存在关联，包括冠状动脉疾病、充血性心力衰竭、动脉高血压、肺动脉高血压、外周动脉疾病、心肌缺血/再灌注相关损伤、中风、心律失常和静脉血栓形成。MPO 水平升高与预后不良相关，包括全因和 CVD 相关死亡率增加的风险增加。MPO 升高至少有两个原因表明 CVD 风险增加。首先，低度炎症和氧化应激与许多代谢异常和合并症并存，因此 MPO 水平升高可能代表一般心血管代谢风险增加。其次，MPO 产生大量高反应性物质，可攻击、破坏或改变每个已知细胞成分的功能。与 CVD 最相关的 MPO 作用是生成具有增加动脉粥样硬化性的功能失调脂蛋白，减少 NO 的可用性、内皮功能障碍、血管反应性受损和动脉粥样硬化斑块不稳定。这些作用强烈表明 MPO 直接参与 CVD 的病理生理学。在这方面，MPO 可以被视为一种介导物或工具，通过它炎症在分子和细胞水平上促进 CVD。MPO 治疗抑制的临床价值仍有待检验。
