Stopping the Primal RAGE Reaction in Myocardial Infarction
- 24 June 2008
- journal article
- editorial
- Published by Wolters Kluwer Health in Circulation
- Vol. 117 (25) , 3165-3167
- https://doi.org/10.1161/circulationaha.108.784397
Abstract
No abstract availableKeywords
This publication has 20 references indexed in Scilit:
- RAGE and Modulation of Ischemic Injury in the Diabetic MyocardiumDiabetes, 2008
- Receptor for Advanced-Glycation End ProductsCirculation, 2006
- Exogenous High-Mobility Group Box 1 Protein Induces Myocardial Regeneration After Infarction via Enhanced Cardiac C-Kit + Cell Proliferation and DifferentiationCirculation Research, 2005
- S100B Expression Modulates Left Ventricular Remodeling After Myocardial Infarction in MiceCirculation, 2005
- RAGE modulates peripheral nerve regeneration via recruitment of both inflammatory and axonal outgrowth pathwaysThe FASEB Journal, 2004
- Antagonism of RAGE suppresses peripheral nerve regenerationThe FASEB Journal, 2004
- Involvement of Toll-like Receptors 2 and 4 in Cellular Activation by High Mobility Group Box 1 ProteinJournal of Biological Chemistry, 2004
- Activation of NADPH oxidase by AGE links oxidant stress to altered gene expression via RAGEAmerican Journal of Physiology-Endocrinology and Metabolism, 2001
- Coregulation of Neurite Outgrowth and Cell Survival by Amphoterin and S100 Proteins through Receptor for Advanced Glycation End Products (RAGE) ActivationJournal of Biological Chemistry, 2000
- RAGE Mediates a Novel Proinflammatory Axis: A Central Cell Surface Receptor for S100/Calgranulin PolypeptidesPublished by Elsevier ,1999