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首页> 外文期刊>Advances in clinical chemistry >Vascular calcification inhibitors in relation to cardiovascular disease with special emphasis on fetuin-A in chronic kidney disease.
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Vascular calcification inhibitors in relation to cardiovascular disease with special emphasis on fetuin-A in chronic kidney disease.

机译：与心血管疾病有关的血管钙化抑制剂，尤其是慢性肾脏疾病中的胎球蛋白A。

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The mortality rate is extremely high in chronic kidney disease (CKD), primarily due to the high prevalence of cardiovascular disease (CVD) in this patient group. Apart from traditional Framingham risk factors, evidences suggest that nontraditional risk factors, such as inflammation, oxidative stress, endothelial dysfunction, and vascular calcification also contribute to this extremely high risk of CVD. Disturbance in the mineral metabolism, especially in the ions of Ca and PO4, are linked to enhanced calcification of blood vessels. Although the mechanism(s) of this enhanced calcification process are not fully understood, current knowledge suggests that a large number (and an imbalance between them) of circulating promoters and inhibitors of the calcification process, that is, fetuin-A (or alpha 2-Heremans-Schmid glycoprotein, AHSG), matrix-Gla protein (MGP), osteoprotegerin (OPG), osteopontin (OPN), bone morphogenetic proteins (BMPs), and inorganic pyrophosphate (PPi), are involved in the deterioration of vascular tissue. Thus, an imbalance in these factors may contribute to the high prevalence of vascular complications in CKD patients. Among these mediators, studies on fetuin-A deserve further attention as clinical studies consistently show that fetuin-A deficiency is associated with vascular calcification, all-cause and cardiovascular mortality in CKD patients. Both chronic inflammation and the uremic milieu per se may contribute to fetuin-A depletion, as well as specific mutations in the AHSG gene. Recent experimental and clinical studies also suggest an intriguing link between fetuin-A, insulin resistance, and the metabolic syndrome.
机译：慢性肾脏病（CKD）的死亡率极高，这主要是由于该患者组的心血管疾病（CVD）患病率很高。除传统的Framingham危险因素外，有证据表明，非传统的危险因素（例如炎症，氧化应激，内皮功能障碍和血管钙化）也导致了这种极高的CVD危险。矿物质代谢的紊乱，尤其是Ca和PO4离子的紊乱，与血管钙化增强有关。尽管尚未完全理解这种增强的钙化过程的机制，但目前的知识表明，大量的循环启动子和钙化过程的抑制剂（即胎球蛋白-A（或alpha 2）（以及它们之间的失衡） -Heremans-Schmid糖蛋白（AHSG），基质Gla蛋白（MGP），骨保护素（OPG），骨桥蛋白（OPN），骨形态发生蛋白（BMP）和无机焦磷酸盐（PPi）参与了血管组织的恶化。因此，这些因素的失衡可能导致CKD患者的血管并发症高发。在这些介体中，有关胎球蛋白-A的研究值得进一步关注，因为临床研究始终显示，胎球蛋白-A缺乏与CKD患者的血管钙化，全因和心血管死亡率有关。慢性炎症和尿毒症环境本身都可能导致胎球蛋白A耗竭，以及AHSG基因的特定突变。最近的实验和临床研究还表明，胎球蛋白-A，胰岛素抵抗和代谢综合征之间存在着有趣的联系。

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