Diabetes and advanced glycation endproducts

被引：628

作者：

Vlassara, H

Palace, MR

机构：

[1] CUNY Mt Sinai Sch Med, Dept Geriatr, Div Expt Diabet & Ageing, New York, NY 10029 USA

[2] CUNY Mt Sinai Sch Med, Dept Med, Div Endocrinol, New York, NY 10029 USA

来源：

JOURNAL OF INTERNAL MEDICINE | 2002年 / 251卷 / 02期

关键词：

D O I：

10.1046/j.1365-2796.2002.00932.x

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Bio-reactive advanced glycation endproducts (AGE) alter the structure and function of molecules in biological systems and increase oxidative stress. These adverse effects of both exogenous and endogenously derived AGE have been implicated in the pathogenesis of diabetic complications and changes associated with ageing including atherosclerosis, renal, eye and neurological disease. Specific AGE receptors and nonreceptor mechanisms contribute to these processes but also assist in the removal and degradation of AGE. The final disposal of AGE depends on renal clearance. Promising pharmacologic strategies to prevent AGE formation, reduce AGE toxicity, and/or inactivate AGE are under investigation.

引用

收藏

页码：87 / 101

页数：15

相关论文

共 147 条

[21] MECHANISTIC STUDIES OF ADVANCED GLYCOSYLATION END-PRODUCT INHIBITION BY AMINOGUANIDINE [J].

EDELSTEIN, D ;

BROWNLEE, M .

DIABETES, 1992, 41 (01) :26-29

[22] PREVENTION OF GLOMERULAR-BASEMENT-MEMBRANE THICKENING BY AMINOGUANIDINE IN EXPERIMENTAL DIABETES-MELLITUS [J].

ELLIS, EN ;

GOOD, BH .

METABOLISM-CLINICAL AND EXPERIMENTAL, 1991, 40 (10) :1016-1019

[23] PROGRESSION OF INCIPIENT DIABETIC-RETINOPATHY DURING GOOD GLYCEMIC CONTROL [J].

ENGERMAN, RL ;

KERN, TS .

DIABETES, 1987, 36 (07) :808-812

[24]

FOGELMAN AM, 1981, J LIPID RES, V22, P1131

[25]

Founds HW, 1996, J INVEST MED, V44, pA200

[26]

GARDINER TA, 1995, LAB INVEST, V72, P439

[27] Aminoguanidine inhibits reactive oxygen species formation, lipid peroxidation, and oxidant-induced apoptosis [J].

Giardino, I ;

Fard, AK ;

Hatchell, DL ;

Brownlee, M .

DIABETES, 1998, 47 (07) :1114-1120

[28] NONENZYMATIC GLYCOSYLATION IN-VITRO AND IN BOVINE ENDOTHELIAL-CELLS ALTERS BASIC FIBROBLAST GROWTH-FACTOR ACTIVITY - A MODEL FOR INTRACELLULAR GLYCOSYLATION IN DIABETES [J].

GIARDINO, I ;

EDELSTEIN, D ;

BROWNLEE, M .

JOURNAL OF CLINICAL INVESTIGATION, 1994, 94 (01) :110-117

[29] Identification of p90, a prominent tyrosine-phosphorylated protein in fibroblast growth factor-stimulated cells, as 80K-H [J].

Goh, KC ;

Lim, YP ;

Ong, SH ;

Siak, CB ;

Cao, XM ;

Tan, YH ;

Guy, GR .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1996, 271 (10) :5832-5838

[30] BINDING-SITE ON MACROPHAGES THAT MEDIATES UPTAKE AND DEGRADATION OF ACETYLATED LOW-DENSITY LIPOPROTEIN, PRODUCING MASSIVE CHOLESTEROL DEPOSITION [J].

GOLDSTEIN, JL ;

HO, YK ;

BASU, SK ;

BROWN, MS .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1979, 76 (01) :333-337

← 1 2 3 4 5 6 7 8 9 10 →