Interaction of carbamylated LDL with LOX-1 in the induction of endothelial dysfunction and atherosclerosis.
Interaction of carbamylated LDL with LOX-1 in the induction of endothelial dysfunction and atherosclerosis.
复制标题
DOI:
10.1093/eurheartj/ehu122
复制
发表时间:
2014-11
影响因子:
39.3
通讯作者:
J. Mehta;A. Basnakian
中科院分区:
文献类型:
--
作者:
J. Mehta;A. Basnakian
This editorial refers to ‘Carbamylated low-density lipoprotein induces endothelial dysfunction’[†][1], by T. Speer et al ., on page 3021. Urea is a normal component of human blood plasma, but it is not inert. Urea-derived cyanate modification of LDL-cholesterol, known as LDL carbamylation, has been discussed for more than a decade.1 Recent studies have linked LDL carbamylation to atherosclerosis in uraemic patients and animals with chronic kidney disease (CKD).2–4 More broadly, protein carbamylation has been linked with atherosclerotic cardiovascular disease (CVD) in CKD.5 Endothelial cell (EC) dysfunction induced by carbamylated LDL (cLDL) seems to be a plausible explanation for the high frequency of CVD in CKD.6 However, despite considerable efforts in determining the mechanistic basis of atherosclerosis induced by cLDL, the link remains blurry since it is hard to relate the complex events based on in vitro , in vivo , and clinical studies done independently. An important contribution by Speer and associates7 is that they were able to combine all these approaches into a unified concept. As opposed to many previous studies which used LDL artificially carbamylated by potassium cyanate, or measured protein carbamylation, or measured plasma cLDL by enzyme-linked immunosorbent assay (ELISA), … [1]: #fn-2