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Journal ArticleDOI

Cellular signalling of the receptor for advanced glycation end products (RAGE).

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TLDR
A comprehensive summary of previous and recent studies relating to the complex molecular network of RAGE signalling, with a particular emphasis on RAGE transgenic mouse models is provided.
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This article is published in Cellular Signalling.The article was published on 2013-11-01. It has received 410 citations till now. The article focuses on the topics: RAGE (receptor) & HMGB1.

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Citations
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The Biological Basis for Cardiac Repair After Myocardial Infarction: From Inflammation to Fibrosis

TL;DR: The renin-angiotensin-aldosterone system and members of the transforming growth factor-β family play an important role in activation of infarct myofibroblasts, and therapeutic modulation of the inflammatory and reparative response may hold promise for the prevention of postinfarction heart failure.
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Complexity of Danger: The Diverse Nature of Damage-associated Molecular Patterns

TL;DR: In this review, the diverse nature, structural characteristics, and signaling pathways elicited by DAMPs will be critically evaluated.
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HMGB1, IL-1α, IL-33 and S100 proteins: dual-function alarmins.

TL;DR: This work has shown that release of alarmins from mesenchymal cells is a highly relevant mechanism by which immune cells can be alerted of tissue damage, and alarmins play a key role in the development of acute or chronic inflammatory diseases and in cancer development.
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Diabetes and Its Effect on Bone and Fracture Healing

TL;DR: Type 1 and type 2 diabetes mellitus impair bone formation under conditions of perturbation such as bacteria-induced periodontal bone loss by increasing osteoblast apoptosis and reducing expression of factors that stimulate osteoblasts such as BMPs and growth factors.
References
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Journal ArticleDOI

Receptor for advanced glycation end products is detrimental during influenza A virus pneumonia

TL;DR: RAGE(-/-) mice were relatively protected from IAV induced mortality and showed an improved viral clearance and enhanced cellular T cell response and activation of neutrophils, suggesting that RAGE is detrimental during IAV pneumonia.
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Receptor for advanced glycation end product (RAGE)-dependent modulation of early growth response-1 in hepatic ischemia/reperfusion injury

TL;DR: Egr-1 was upregulated in the liver remnants after hepatic I/R injury and was suppressed by administration of soluble RAGE or deletion of the RAGE gene, which may contribute to the protective mechanisms underlying the beneficial impact of RAGE blockade or deletion.
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Receptors for advanced glycation end-products targeting protect against hyperoxia-induced lung injury in mice

TL;DR: Data reveal that RAGE targeting leads to a diminished hyperoxia-induced pulmonary inflammatory response, and further research into the role of RAGE signaling in the lung should identify novel targets likely to be important in the therapeutic alleviation of lung injury and associated persistent inflammation.
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HMGB1-RAGE regulates muscle satellite cell homeostasis through p38-MAPK- and myogenin-dependent repression of Pax7 transcription.

TL;DR: RAGE signaling physiologically repressed Pax7 transcription in SCs by upregulating myogenin, thereby accelerating muscle regeneration and limiting SC self-renewal, and was transiently expressed in activated, proliferating and differentiating satellite cells (SCs) in injured muscles.
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Complement C3a, CpG Oligos, and DNA/C3a Complex Stimulate IFN-α Production in a Receptor for Advanced Glycation End Product-Dependent Manner

TL;DR: C3a and CpGA synergize to increase IFN-α production in a RAGE-dependent manner and stimulate an innate immune response and indicate a potential role of RAGE in autoimmune diseases that show accumulation of immunostimulatory DNA and C3a.
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