Activation of NADPH oxidase by AGE links oxidant stress to altered gene expression via RAGE.

By M. Wautier, O. Chappey, S. Corda, D. Stern, A. Schmidt, J. Wautier. American Journal of Physiology. Endocrinology and Metabolism, 2001

1,088 citations recorded by the source corpus.

Subfields: Clinical Biochemistry, Immunology, Nephrology

View Paper: https://www.semanticscholar.org/paper/9df8cf6024095f9977fbc8afff4458df29947b79

How researchers see this paper

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In Clinical Biochemistry

1. George Perry
2. C. van Dijk
3. T. Berl

In Immunology

1. R. Clempus
2. B. Lassègue
3. A. Shah
4. George Perry
5. Mark A. Smith
6. Jian-Mei Li
7. Rhian M. Touyz
8. E. Schiffrin

Citations in the corpus

• Understanding RAGE, the receptor for advanced glycation end products (2005, background): “In addition, RAGE–ligand interaction may directly induce generation of reactive oxygen species via NADPH oxidases and/or other identified mechanisms [11, 52].”
• Advanced Glycation End-Products (AGEs): Formation, Chemistry, Classification, Receptors, and Diseases Related to AGEs (2022, background): “It was demonstrated that the AGE– RAGE axis activated NADPH oxidase in mouse cells, which increased oxidative stress and inhibited transcription factor activity [155].”
• Mechanisms of diabetic complications. (2013, background): “This is most likely due to RAGE modulation being upstream of many important pathological pathways relevant to diabetic complications, including ROS generation (122, 636), activation of the immune system (30, 90, 92), release of cytokines (191), and a newly discovered role in glycemic control (78, 12”
• Vascular NAD(P)H oxidases: specific features, expression, and regulation. (2003, background): “Several in vitro studies have shown that high glucose and advanced glycation end products increase ROS formation in VSMC (84), endothelial cells (218), and isolated arterial segments (31).”
• Cardiovascular actions of insulin. (2007, background): “AGEs also enhance expression of ET-1 in endothelial cells through the activation of NF- B (255).”
• Advanced glycation end products and vascular inflammation: implications for accelerated atherosclerosis in diabetes. (2004, background): “In the vasculature, the principal pathological consequence of AGE interaction with endothelial surface RAGE is the induction of intracellular reactive oxygen species (ROS) [58], the generation of which seems to be linked, at least in part, to the activation of the NAD(P)H-oxidase system [59] (Fig.”
• Pathogenesis of Diabetic Nephropathy (2004, positive): “Interactions of AGEs with RAGE to generate reactive oxygen species (ROS) have been implicated as a mechanism underlying these findings [52].”
• NADPH Oxidases in Cardiovascular Health and Disease (2006, neutral): “Under these conditions, interstitial fibroblasts transform into myofibroblasts that express (cid”
• Endothelial cell superoxide generation: regulation and relevance for cardiovascular pathophysiology. (2004, background): “These include hyperinsulinemia (76), elevated blood glucose and free fatty acids (34, 69), hypercholesterolemia (133, 144, 148), increased AGEs (164, 177), and increased activation of the renin-angiotensin system (98, 176).”
• Advanced glycation end products and RAGE: a common thread in aging, diabetes, neurodegeneration, and inflammation. (2005, background): “A large body of evidence suggests that one consequence of AGE–RAGE interaction is the generation of ROS, at least in part via the activation of NADPH oxidase (Yan et al., 1994; Lander et al., 1997; Wautier et al., 2001), although other sources of ROS dependent upon RAGE have not been ruled out.”
• Diabetes-associated sustained activation of the transcription factor nuclear factor-kappaB. (2001, background): “A recent study demonstrated that upon AGE engagement of RAGE, NADPH-oxidase is one major source of ROS in endothelial cells (105) and thus implicates that multiple sources of oxidative stress contribute to RAGE-mediated NF- B activation (43,105).”