Advanced Glycosylation End Products

Products derived from the nonenzymatic reaction of glucose and proteins in vivo that exhibit a yellow-brown pigmentation and an ability to participate in protein-protein cross-linking. These substances are involved in biological processes relating to protein turnover and it is believed that their excessive accumulation contributes to the chronic complications of diabetes mellitus.

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Networked: 2322 relevant articles (22 outcomes, 156 trials/studies)

Relationship Network

Bio-Agent Context: Research Results

Experts

1.	Yamagishi, Sho-ichi: 81 articles (05/2015 - 06/2002)
2.	Takeuchi, Masayoshi: 74 articles (12/2015 - 06/2002)
3.	Matsui, Takanori: 61 articles (05/2015 - 03/2006)
4.	Yamagishi, S: 39 articles (08/2015 - 08/2000)
5.	Schmidt, Ann Marie: 38 articles (10/2014 - 02/2002)
6.	Takeuchi, M: 30 articles (05/2015 - 01/2001)
7.	Cooper, Mark E: 28 articles (01/2014 - 09/2002)
8.	Yamagishi, Sho-Ichi: 26 articles (12/2015 - 02/2003)
9.	Schalkwijk, Casper G: 26 articles (08/2015 - 01/2002)
10.	Vlassara, Helen: 26 articles (05/2015 - 07/2002)

Related Diseases

1.	Inflammation 10/01/2014 - "cAMP ameliorates inflammation by modulation of macrophage receptor for advanced glycation end-products." 10/15/2014 - "S100A12 binds to the receptor of advanced glycation end products (RAGE), a pattern-recognition receptor, and results of studies in human patients with IBD and other conditions suggest a role of RAGE in chronic inflammation. " 01/01/2014 - "Although several studies showed that decreased soluble receptor for advanced glycation end products (sRAGE) is associated with metabolic syndrome (MetS), inflammation level has not been considered, even though ligand-RAGE interaction induces inflammation. " 01/01/2013 - "Our study suggests that the renal protective role of XXD with multiple effective ingredients involves inhibition of inflammation through downregulation of the nuclear factor- κ B pathway, reducing renal advanced glycation end-products and receptor for advanced glycation end-product in diabetic rats. " 06/14/2012 - "Recent studies suggested that advanced glycation end-products (AGEs) and their receptor (RAGE) interaction may be promoted by inflammation and oxidative stress. "
2.	Diabetic Nephropathies (Diabetic Nephropathy) 01/01/2014 - "In our study, we hypothesized that receptors for advanced glycation end-products (RAGE) mediate endoplasmic reticulum (ER) stress to induce premature senescence via p21 signaling activation in diabetic nephropathy. " 03/01/2010 - "Advanced glycation end products (AGEs) and the receptor for AGEs (RAGE) generate ROS, and therefore this study evaluated the effects of RAGE deletion, decreasing AGE accumulation, or lowering dietary AGE content on oxidative parameters in diabetic nephropathy (DN). " 01/01/2004 - "Randomized trial of an inhibitor of formation of advanced glycation end products in diabetic nephropathy." 10/01/1991 - "This study evaluated the relationship between the development of fluorescence related to advanced glycosylation end products (AGEs) in the kidney and experimental diabetic nephropathy over a 32-wk period. " 02/01/2016 - "Advanced glycation end products (AGEs), inflammatory-activated macrophages are essential in the initiation and progression of diabetic nephropathy (DN). "
3.	Chronic Kidney Failure (Chronic Renal Failure) 01/01/2002 - "Previous studies have demonstrated the accumulation of advanced glycation end products (AGE) in patients with chronic renal failure (CRF), but the mechanism is not completely understood. " 12/01/1994 - "Immunohistochemical study of human advanced glycosylation end-products (AGE) in chronic renal failure." 01/01/2014 - "Advanced glycation end-products and skin autofluorescence in end-stage renal disease: a review." 10/01/2011 - "Cardiovascular and connective tissue disorders are very common in patients with end-stage renal disease, and the accumulation of advanced glycation end-products is significantly increased in these patients. " 04/01/2011 - "Thus, tissue accumulated, but not circulating, advanced glycation end products may be a determinant of a decrease in circulating EPCs in ESRD subjects."
4.	Diabetic Angiopathies (Diabetic Angiopathy) 05/01/2000 - "Cross-link breakers seem to be effective in preventing or reversing accumulation of advanced glycation end-products in blood vessels and have the potential to play a part in the treatment of diabetic vascular complications." 07/01/2009 - "Many studies have demonstrated association between advanced glycation end products (AGEs) and diabetic angiopathy. " 03/28/1997 - "This study was undertaken to determine whether and how advanced glycation end products (AGE), senescent macroproteins accumulated in various tissues under hyperglycemic states, cause angiogenesis, the principal vascular derangement in diabetic microangiopathy. " 09/01/2015 - "Advanced glycation end products (AGEs) play an important role in the pathogenesis of diabetic vascular complications. " 01/01/2015 - "Advanced glycation end-products (AGEs) are thought to play a major role in the pathogenesis of diabetic vascular complications. "
5.	Atherosclerosis 09/15/2007 - "Infusion of the soluble form of the receptor for advanced glycation end-products (sRAGE) was protective against atherosclerosis and nephropathy in animal models. " 01/01/2015 - "Genetics of Plasma Soluble Receptor for Advanced Glycation End-Products and Cardiovascular Outcomes in a Community-based Population: Results from the Atherosclerosis Risk in Communities Study." 07/01/2009 - "Association between circulating soluble receptor for advanced glycation end products and atherosclerosis: observations from the Dallas Heart Study." 06/01/2005 - "Advanced glycation end products in diabetes-associated atherosclerosis and renal disease: interventional studies." 10/29/1999 - "Recent studies suggested that interruption of the interaction of advanced glycation end products (AGEs), with the signal-transducing receptor receptor for AGE (RAGE), by administration of the soluble, extracellular ligand-binding domain of RAGE, reversed vascular hyperpermeability and suppressed accelerated atherosclerosis in diabetic rodents. "

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