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RAGE Mediates a Novel Proinflammatory Axis A Central Cell Surface Receptor for S100/Calgranulin Polypeptides
TLDR
It is reported here that receptor for AGE (RAGE) is a central cell surface receptor for EN-RAGE (extracellular newly identified RAGE-binding protein) and related members of the S100/calgranulin superfamily. Expand
Toll-like receptor 9–dependent activation by DNA-containing immune complexes is mediated by HMGB1 and RAGE
TLDR
HMGB1, a nuclear DNA-binding protein released from necrotic cells, was an essential component of DNA-containing immune complexes that stimulated cytokine production through a TLR9–MyD88 pathway involving the multivalent receptor RAGE. Expand
Understanding RAGE, the receptor for advanced glycation end products
TLDR
Administration of the receptor decoy, sRAGE, is likely to sequester ligands, thereby preventing their interaction with other receptors in addition to RAGE, suggesting that, just as RAGE is a multiligand receptor, its ligands are also likely to recognize several receptors in mediating their biologic effects. Expand
A critical cysteine is required for HMGB1 binding to Toll-like receptor 4 and activation of macrophage cytokine release
TLDR
It is shown that Toll-like receptor 4 (TLR4), a pivotal receptor for activation of innate immunity and cytokine release, is required for HMGB1-dependent activation of macrophage TNF release. Expand
A mechanism converting psychosocial stress into mononuclear cell activation
TLDR
Noradrenaline-dependent adrenergic stimulation results in activation of NF-κB in vitro and in vivo, which represents a downstream effector for the neuroendocrine response to stressful psychosocial events and links changes in the activity of the neuro endocrine axis to the cellular response. Expand
The Pattern Recognition Receptor (RAGE) Is a Counterreceptor for Leukocyte Integrins
TLDR
It is shown that RAGE functions as an endothelial adhesion receptor promoting leukocyte recruitment relevant in inflammatory disorders associated with increased RAGE expression, such as in diabetes, and could provide the basis for the development of novel therapeutic applications. Expand
High-Mobility Group Box-1 in Ischemia-Reperfusion Injury of the Heart
TLDR
It is demonstrated that HMGB1 acts as an early mediator of inflammation and organ damage in I/R injury of the heart by binding to RAGE, resulting in the activation of proinflammatory pathways and enhanced myocardial injury. Expand
The HMGB1 Receptor RAGE Mediates Ischemic Brain Damage
TLDR
Evidence is provided that the receptor for advanced glycation end products (RAGE) functions as a sensor of necrotic cell death and contributes to inflammation and ischemic brain damage in stroke and HMGB1–RAGE signaling may provide a target for anti-inflammatory therapy in stroke. Expand
Diabetes-associated sustained activation of the transcription factor nuclear factor-kappaB.
TLDR
Data demonstrate that ligands of RAGE can induce sustained activation of NF-kappaB as a result of increased levels of de novo synthesized NF-KappaBp65 overriding endogenous negative feedback mechanisms and thus might contribute to the persistent NF- kappaB activation observed in hyperglycemia and possibly other chronic diseases. Expand
Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy
TLDR
In retinas of diabetic animals, benfotiamine treatment inhibited these three pathways and NF-κB activation by activating transketolase, and also prevented experimental diabetic retinopathy, which might be clinically useful in preventing the development and progression of diabetic complications. Expand
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