The Role of Nonenzymatic Post-translational Protein Modifications in Uremic Vascular Calcification.
The Role of Nonenzymatic Post-translational Protein Modifications in Uremic Vascular Calcification.
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DOI：
10.1053/j.ackd.2019.10.001
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发表时间：
2019-11
影响因子：
2.9
通讯作者：
Kenneth Lim;Sahir Kalim
中科院分区：
文献类型：
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作者：
Kenneth Lim;Sahir Kalim
巨大的技术进步使得非酶翻译后修饰蛋白的鉴定和与肾衰竭患者心血管疾病（CVD）发病机制的联系成为可能。通过非酶促氨甲酰化反应以及高级糖基化终产物的形成等过程，我们现在知道蛋白质修饰始终与CVD的发展相关，而不仅仅是一种附带现象，这已成为近年来肾脏病学研究的重要焦点。尽管肾衰竭中发生的蛋白质修饰可能导致CVD的具体机制多种多样，包括炎症和纤维化等途径，但血管钙化已成为蛋白质修饰的独特病理后遗症。在这篇综述中，我们考虑了蛋白质氨甲酰化和晚期糖基化终产物在 CVD 发展中的生物学机制和临床相关性，重点关注血管钙化。
Considerable technological advances have enabled the identification and linkage of nonenzymatic post-translationally modified proteins to the pathogenesis of cardiovascular disease (CVD) in patients with kidney failure. Through processes such as the nonenzymatic carbamylation reaction as well as the formation of advanced glycation end products, we now know that protein modifications are invariably associated with the development of CVD beyond a mere epiphenomenon and this has become an important focus of nephrology research in recent years. Although the specific mechanisms by which protein modifications occurring in kidney failure that may contribute to CVD are diverse and include pathways such as inflammation and fibrosis, vascular calcification has emerged as a distinct pathological sequelae of protein modifications. In this review, we consider the biological mechanisms and clinical relevance of protein carbamylation and advanced glycation end products in CVD development with a focus on vascular calcification.