Homocysteine in Renal Injury

被引:94
作者
Long, Yanjun [1 ,2 ]
Nie, Jing [1 ]
机构
[1] Southern Med Univ, Natl Clin Res Ctr Kidney Dis, Div Nephrol, State Key Lab Organ Failure Res,Nanfang Hosp, Guangzhou, Guangdong, Peoples R China
[2] Guizhou Prov Peoples Hosp, Guizhou Prov Inst Nephrit & Urinary Dis, Div Nephrol, Guiyang, Guizhou, Peoples R China
关键词
Hyperhomocysteinemia; Chronic kidney disease; Oxidative stress; Endoplasmic reticulum stress; Hypomethylation; CHRONIC KIDNEY-DISEASE; VASCULAR ENDOTHELIAL-CELLS; S-ADENOSYLHOMOCYSTEINE; METHIONINE METABOLISM; PLASMA HOMOCYSTEINE; ARTERIAL STIFFNESS; SERUM HOMOCYSTEINE; GENERAL-POPULATION; RISK-FACTOR; HYPERHOMOCYSTEINEMIA;
D O I
10.1159/000444900
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Background: Homocysteine (Hcy) is an intermediate of methionine metabolism. Hyperhomocysteinemia (HHcy) can result from a deficiency in the enzymes or vitamin cofactors required for Hcy metabolism. Patients with renal disease tend to be hyperhomocysteinemic, particularly as renal function declines, although the underlying cause of HHcy in renal disease is not entirely understood. Summary: HHcy is considered a risk or pathogenic factor in the progression of chronic kidney disease (CKD) as well as the cardiovascular complications. Key Messages: In this review, we summarize both clinical and experimental findings that reveal the contribution of Hcy as a pathogenic factor to the development of CKD. In addition, we discuss several important mechanisms mediating the pathogenic action of Hcy in the kidney, such as local oxidative stress, endoplasmic reticulum stress, inflammation and hypomethylation. (C) 2016 S. Karger AG, Basel
引用
收藏
页码:80 / 87
页数:8
相关论文
共 63 条
[1]   Homocysteine-induced changes in mRNA levels of genes coding for cytoplasmic- and endoplasmic reticulum-resident stress proteins in neuronal cell cultures [J].
Althausen, S ;
Paschen, W .
MOLECULAR BRAIN RESEARCH, 2000, 84 (1-2) :32-40
[2]   Influence of biochemical alterations on arterial stiffness in patients with end-stage renal disease [J].
Blacher, J ;
Demuth, K ;
Guerin, AP ;
Safar, ME ;
Moatti, N ;
London, GM .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 1998, 18 (04) :535-541
[3]  
Bolander-Gouaille C, 2001, FOCUS HOMOCYSTEINE V
[4]   Hyperhomocysteinemia in end-stage renal disease: Prevalence, etiology, and potential relationship to arteriosclerotic outcomes [J].
Bostom, AG ;
Lathrop, L .
KIDNEY INTERNATIONAL, 1997, 52 (01) :10-20
[5]   Homocysteine-responsive ATF3 gene expression in human vascular endothelial cells:: activation of c-Jun NH2-terminal kinase and promoter response element [J].
Cai, Y ;
Zhang, C ;
Nawa, T ;
Aso, T ;
Tanaka, M ;
Oshiro, S ;
Ichijo, H ;
Kitajima, S .
BLOOD, 2000, 96 (06) :2140-2148
[6]  
Cheung GTY, 2008, CAN J PHYSIOL PHARM, V86, P88, DOI [10.1139/Y08-002, 10.1139/y08-002]
[7]   HOMOCYSTEINE EXPORT FROM CELLS CULTURED IN THE PRESENCE OF PHYSIOLOGICAL OR SUPERFLUOUS LEVELS OF METHIONINE - METHIONINE LOADING OF NONTRANSFORMED, TRANSFORMED, PROLIFERATING, AND QUIESCENT CELLS IN CULTURE [J].
CHRISTENSEN, B ;
REFSUM, H ;
VINTERMYR, O ;
UELAND, PM .
JOURNAL OF CELLULAR PHYSIOLOGY, 1991, 146 (01) :52-62
[8]   Prevalence of low glomerular filtration rate in nondiabetic Americans: Third National Health and Nutrition Examination Survey (NHANES III) [J].
Clase, CM ;
Garg, AX ;
Kiberd, BA .
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, 2002, 13 (05) :1338-1349
[9]  
Craig SAS, 2004, AM J CLIN NUTR, V80, P539
[10]   Histone modification and the control of heterochromatic gene silencing in Drosophila [J].
Ebert, Anja ;
Lein, Sandro ;
Schotta, Gunnar ;
Reuter, Gunter .
CHROMOSOME RESEARCH, 2006, 14 (04) :377-392