Roles of the Receptor for Advanced Glycation Endproducts in Diabetes-Induced Vascular Injury
Open Access
- 1 January 2005
- journal article
- review article
- Published by Japanese Pharmacological Society in Journal of Pharmacological Sciences
- Vol. 97 (3) , 305-311
- https://doi.org/10.1254/jphs.cpj04005x
Abstract
Japan's largest platform for academic e-journals: J-STAGE is a full text database for reviewed academic papers published by Japanese societiesKeywords
This publication has 32 references indexed in Scilit:
- Protein GlycationCirculation Research, 2004
- RAGE AxisArteriosclerosis, Thrombosis, and Vascular Biology, 2004
- Regulation of monocyte migration by amphoterin (HMGB1)Blood, 2004
- The AGE-RAGE System and Diabetic NephropathyJournal of the American Society of Nephrology, 2003
- Biochemistry and molecular cell biology of diabetic complicationsNature, 2001
- Ribozyme Targeting of Receptor for Advanced Glycation End Products in Mouse Mesangial CellsBiochemical and Biophysical Research Communications, 1998
- Advanced glycosylation end products stimulate the growth but inhibit the prostacyclin‐producing ability of endothelial cells through interactions with their receptorsFEBS Letters, 1996
- Receptor-Mediated Toxicity to Pericytes of Advanced Glycosylation End Products: A Possible Mechanism of Pericyte Loss in Diabetic MicroangiopathyBiochemical and Biophysical Research Communications, 1995
- Vascular Pericytes Not Only Regulate Growth, but Also Preserve Prostacyclin-Producing Ability and Protect Against Lipid Peroxide-Induced Injury of Cocultured Endothelial CellsBiochemical and Biophysical Research Communications, 1993
- Advanced Glycosylation End Products in Tissue and the Biochemical Basis of Diabetic ComplicationsNew England Journal of Medicine, 1988