Atherosclerosis in Chronic Kidney Disease: Lessons Learned from Glycation in Diabetes

被引：17
作者：
Mohar, Dilbahar S. [1 ,2 ]
Barseghian, Ailin [1 ,2 ]
Haider, Nezam [1 ,2 ]
Domanski, Michael [1 ,2 ]
Narula, Jagat [1 ,2 ]
机构：
[1] Univ Calif Irvine, Div Cardiol, Sch Med, Orange, CA 92868 USA
[2] Mt Sinai Sch Med, New York, NY 10029 USA
来源：
MEDICAL CLINICS OF NORTH AMERICA | 2012年 / 96卷 / 01期
关键词：
Glycation; Carbamylation; Advanced glycated end products; Atherosclerosis; Cardiovascular disease; LOW-DENSITY-LIPOPROTEIN; NON-ENZYMATIC GLUCOSYLATION; HUMAN BLOOD MONOCYTES; CARBAMYLATED HEMOGLOBIN; ENDOTHELIAL-CELLS; END-PRODUCTS; IN-VITRO; NONENZYMATIC GLYCOSYLATION; DECREASED CLEARANCE; GLUCOSE CONTROL;
D O I：
10.1016/j.mcna.2011.11.005
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
In diabetes, glycation is a nonenzymatic posttranslational modification resulting from the bonding of a sugar molecule with a protein or lipid followed by oxidation, resulting in the development of advanced glycation end products (AGE). Like glycation, carbamylation is a posttranslational protein modification that is associated with AGE formation. Glycation of extracellular matrix proteins and low-density lipoprotein with subsequent deposition in the vessel wall could contribute to inflammatory response and atheroma formation. It is logical to extrapolate that carbamylation may result in modification of vessel wall proteins similar to glycation, and predispose to atherosclerosis.
引用
收藏
页码：57 / +
页数：10
相关论文
共 56 条
123456