氰酸盐在尿毒症期间诱导血管功能障碍中的作用：不仅仅是蛋白质的氨甲酰化作用？

Role of cyanate in the induction of vascular dysfunction during uremia: more than protein carbamylation?

机构信息

1] Heart Research Institute, Newtown, New South Wales, Australia [2] Sydney Medical School, University of Sydney, Sydney, New South Wales, Australia.

出版信息

Kidney Int. 2014 Nov;86(5):875-7. doi: 10.1038/ki.2014.256.

DOI:10.1038/ki.2014.256

PMID:25360490

Abstract

Cyanate is a uremic toxin responsible for the carbamylation of proteins, which has been implicated as playing a key role in accelerating the progression of atherosclerosis in patients with chronic kidney disease. El-Gamal et al. report that while cyanate promotes protein carbamylation in vivo, the resulting endothelial dysfunction observed is consistent with reactions mediated by cyanate itself, rather than by carbamylated proteins. This provides new insight into the relationship between uremia and cardiovascular disease.

摘要

氰酸盐是一种尿毒症毒素，可导致蛋白质发生氨甲酰化，这被认为在加速慢性肾脏病患者动脉粥样硬化进展方面起着关键作用。El-Gamal 等人报告说，虽然氰酸盐可促进体内蛋白质的氨甲酰化，但观察到的内皮功能障碍与氰酸盐本身介导的反应一致，而不是与氨甲酰化蛋白有关。这为尿毒症与心血管疾病之间的关系提供了新的见解。