McNair Erick D, Wells Calvin R, Qureshi A M, Pearce Colin, Caspar-Bell Gudrun, Prasad Kailash
Int J Angiol. 2011 Mar;20(1):49-54. doi: 10.1055/s-0031-1272552.
Interaction of advanced glycation end products (AGEs) with the receptor for advanced AGEs (RAGE) results in activation of nuclear factor kappa-B, release of cytokines, expression of adhesion molecules, and induction of oxidative stress. Oxygen radicals are involved in plaque rupture contributing to thromboembolism, resulting in acute coronary syndrome (ACS). Thromboembolism and the direct effect of oxygen radicals on myocardial cells cause cardiac damage that results in the release of cardiac troponin-I (cTnI) and other biochemical markers. The soluble RAGE (sRAGE) compete with RAGE for binding with AGE, thus functioning as a decoy and exerting a cytoprotective effect. Low levels of serum sRAGE would allow unopposed serum AGE availability for binding with RAGE, resulting in the generation of oxygen radicals and proinflammatory molecules that have deleterious consequences and promote myocardial damage. sRAGE may stabilize atherosclerotic plaques. It is hypothesized that low levels of sRAGE are associated with high levels of serum cTnI in patients with ACS. The main objective of the study was to determine whether low levels of serum sRAGE are associated with high levels of serum cTnI in ACS patients. The serum levels of sRAGE and cTnI were measured in 36 patients with non-ST-segment elevation myocardial infarction (NSTEMI) and 30 control subjects. Serum levels of sRAGE were lower in NSTEMI patients (802.56 ± 39.32 pg/mL) as compared with control subjects (1311.43 ± 66.92 pg/mL). The levels of cTnI were higher in NSTEMI patients (2.18 ± 0.33 μg/mL) as compared with control subjects (0.012 ± 0.001 μg/mL). Serum sRAGE levels were negatively correlated with the levels of cTnI. In conclusion, the data suggest that low levels of serum sRAGE are associated with high serum levels of cTnI and that there is a negative correlation between sRAGE and cTnI.
晚期糖基化终末产物（AGEs）与晚期糖基化终末产物受体（RAGE）相互作用会导致核因子κB激活、细胞因子释放、黏附分子表达以及氧化应激诱导。氧自由基参与斑块破裂，促成血栓栓塞，进而导致急性冠状动脉综合征（ACS）。血栓栓塞以及氧自由基对心肌细胞的直接作用会造成心脏损伤，导致心肌肌钙蛋白I（cTnI）及其他生化标志物的释放。可溶性RAGE（sRAGE）与RAGE竞争结合AGE，从而起到诱饵作用并发挥细胞保护效应。血清sRAGE水平较低会使血清AGE不受阻碍地与RAGE结合，导致氧自由基和促炎分子生成，产生有害后果并促进心肌损伤。sRAGE可能会使动脉粥样硬化斑块稳定。据推测，ACS患者血清sRAGE水平较低与血清cTnI水平较高有关。该研究的主要目的是确定ACS患者血清sRAGE水平较低是否与血清cTnI水平较高有关。对36例非ST段抬高型心肌梗死（NSTEMI）患者和30例对照受试者的血清sRAGE和cTnI水平进行了测量。与对照受试者（1311.43±66.92 pg/mL）相比，NSTEMI患者的血清sRAGE水平较低（802.56±39.32 pg/mL）。与对照受试者（0.012±0.001 μg/mL）相比，NSTEMI患者的cTnI水平较高（2.18±0.33 μg/mL）。血清sRAGE水平与cTnI水平呈负相关。总之，数据表明血清sRAGE水平较低与血清cTnI高水平有关，且sRAGE与cTnI之间存在负相关。
