Understanding RAGE, the receptor for advanced glycation end products

By A. Bierhaus, P. Humpert, M. Morcos, T. Wendt, T. Chavakis, B. Arnold, D. Stern, P. Nawroth. Journal of molecular medicine, 2005

1,312 citations recorded by the source corpus.

Subfields: Clinical Biochemistry, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/726ac389b7698420c10ac71885f22827aeed7ed5

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Clinical Biochemistry

1. A. Manfredi
2. M. Bianchi

In Molecular Biology

1. A. Manfredi
2. S. Biswas
3. M. Bianchi
4. W. Dichtl
5. T. Senoner

Citations in the corpus

• Diabetes and vascular disease: pathophysiology, clinical consequences, and medical therapy: part I (2013, background): “ation of AGEs leads to cellular dysfunction by eliciting activation of the AGEs receptor (RAGE).(30,32) AGE-RAGE signalling in turn acti-”
• Diabetes and Vascular Disease: Pathophysiology, Clinical Consequences, and Medical Therapy: Part I (2003, background): “ation of AGEs leads to cellular dysfunction by eliciting activation of the AGEs receptor (RAGE).(30,32) AGE-RAGE signalling in turn acti-”
• Dietary factors and low-grade inflammation in relation to overweight and obesity (2011, neutral): “ROS can trigger proinflammatory signalling pathways causing MAPK-dependent activation of transcription factors such as NF-kB and consequent modulation of the gene expression of several pro-inflammatory cytokines((474,475,477)).”
• DAMPs, PAMPs and alarmins: all we need to know about danger (2007, background): “RAGE is a multiligand receptor binding advanced glycation end products (AGEs), some S100s, amyloid peptide and HMGB1 [39].”
• Advanced Glycation End Products and Diabetes Mellitus: Mechanisms and Perspectives (2022, background): “AGEs can modulate cellular functions through binding with Toll-like receptors, scavenger receptors, G-protein-coupled receptors, and pattern recognition receptors [12,37].”
• S100A8 and S100A9 in inflammation and cancer. (2006, background): “receptor–ligand interaction indicated that RAGE recognizes three-dimensional structures rather than specific amino acid sequences, and therefore, RAGE could be considered as a pattern recognition receptor [128].”
• Oxidative Stress in Cardiovascular Diseases: Still a Therapeutic Target? (2019, background): “Interaction of advanced glycation end products (AGEs) and its receptor (RAGE) initiates a signaling cascade that activates the transcription factor NF-κB, inducing oxidative stress and leading to an expanded release of inflammatory cytokines such as TNF-α, thus AGEs and RAGE are recognized as oxidat”
• Oxidative Stress in Aging Human Skin (2015, background): “transcription of pro-inflammatory genes and RAGE themselves leading to a vicious cycle [269].”
• Does the Interdependence between Oxidative Stress and Inflammation Explain the Antioxidant Paradox? (2016, background): “These factors act in combinatorial and cell-specific manner to induce proinflammatory gene expression, exert antimicrobial functions, and recruit additional immune cells [44, 45].”
• Functions of S100 Proteins (2012, background): “However, in a background of inflammation and/or neurodegenerative disorders, which is accompanied by enhanced expression levels of S100B and the S100B receptor, RAGE, in neural and inflammatory cells [7,320-322], S100B acts synergistically with proinflammatory cytokines and, at higher concentrations”
• High‐mobility group box 1 (HMGB1) protein at the crossroads between innate and adaptive immunity (2007, background): “RAGE is also a receptor for some S100 proteins, for b-fibrils involved in Alzheimer’s disease, and for advanced glycation end products (41).”