Lowering of dietary advanced glycation endproducts (AGE) reduces neointimal formation after arterial injury in genetically hypercholesterolemic mice
Authors:
- Reigh-Yi LinRLReigh-Yi Lin
- Ernane D ReisERErnane D Reis
- Anthony T DoreADAnthony T Dore
- Min LuMLMin Lu
- Newsha GhodsiNGNewsha Ghodsi
- John T FallonJohn T Fallon
- Edward A FisherEFEdward A Fisher
- Helen VlassaraHVHelen Vlassara
- 1 August 2002
- journal article
- Published by Elsevier in Atherosclerosis
- Vol. 163 (2) , 303-311
Abstract
No abstract availableKeywords
This publication has 28 references indexed in Scilit:
- Differential expression of renal AGE-receptor genes in NOD mice: Possible role in nonobese diabetic renal diseaseKidney International, 2000
- Mouse Models of AtherosclerosisScience, 1996
- Advanced glycosylation end products in diabetic renal and vascular diseaseAmerican Journal of Kidney Diseases, 1995
- Advanced glycation endproducts interacting with their endothelial receptor induce expression of vascular cell adhesion molecule-1 (VCAM-1) in cultured human endothelial cells and in mice. A potential mechanism for the accelerated vasculopathy of diabetes.Journal of Clinical Investigation, 1995
- Serum Advanced Glycosylation End Products: A New Class of Uremic Toxins?Blood Purification, 1994
- Hemoglobin-AGE: A Circulating Marker of Advanced GlycosylationScience, 1992
- Severe hypercholesterolemia and atherosclerosis in apolipoprotein E-deficient mice created by homologous recombination in ES cellsCell, 1992
- Endothelial receptor-mediated binding of glucose-modified albumin is associated with increased monolayer permeability and modulation of cell surface coagulant properties.Journal of Experimental Medicine, 1989
- Advanced Glycosylation End Products in Tissue and the Biochemical Basis of Diabetic ComplicationsNew England Journal of Medicine, 1988
- Protein glycosylation and the pathogenesis of atherosclerosisMetabolism, 1985