RAGE drives the development of glomerulosclerosis and implicates podocyte activation in the pathogenesis of diabetic nephropathy.

By T. Wendt, N. Tanji, Jiancheng Guo, T. Kislinger, W. Qu, Yan Lu, L. Bucciarelli, L. Rong, B. Moser, G. Markowitz and 8 more. American Journal of Pathology, 2003

631 citations recorded by the source corpus.

Subfields: Clinical Biochemistry, Nephrology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/bd8490147680c2ef745f46a79572fd58a854f7ff

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In Pulmonary and Respiratory Medicine

1. J. Forbes
2. M. Cooper

Citations in the corpus

• Oxidative Stress as a Major Culprit in Kidney Disease in Diabetes (2008, background): “Previously, cytosolic generation of ROS has been demonstrated in vitro through activation of the RAGE receptor in both proximal tubular and mesangial cells, most likely through NAD(P)H oxidase (33).”
• Advanced glycation end products and RAGE: a common thread in aging, diabetes, neurodegeneration, and inflammation. (2005, background): “AGEs and their precursors (methylglyoxal and glyoxal) may increased the aggregation and cytotoxicity of intracellular amyloid-beta carboxy-terminal fragments (Woltjer et al., 2003).”
• Mechanisms of diabetic complications. (2013, background): “Administration of soluble RAGE or RAGE-neutralizing antibodies (181) in rodent models of diabetes have also shown protection against complications, which is also seen in RAGE-deficient mice (122, 407, 551, 578, 639).”
• The Pattern Recognition Receptor (RAGE) Is a Counterreceptor for Leukocyte Integrins (2003, methodology): “RAGE is a central player in inflammation (5) and in diabetic complications (5, 20) and our findings help to clarify its functional role.”
• Advanced Glycation End Products and Diabetes Mellitus: Mechanisms and Perspectives (2022, background): “AGEs are metabolic mediators of kidney damage as its correspondent receptor RAGE is expressed by several cell types in the kidney as podocytes [110], tubular epithelial cells, and mesangial cells [84,88].”
• Molecular mechanisms of diabetic kidney disease. (2014, neutral): “Hyperglycemia also increases the non-enzymatic reaction of glucose and other glycating compounds derived both from glucose and from increased fatty acid oxidation, which generates advanced glycation end products in complication-prone cell types, including kidney cells (36).”
• Mouse models of diabetic nephropathy. (2005, background): “It is interesting that neutralizing soluble RAGE ameliorated glomerular damage in the hyperglycemic db/db mouse (220).”
• Dietary factors and low-grade inflammation in relation to overweight and obesity (2011, positive): “In addition, RAGE ablation prevented diabetic nephropathy((493)) and neuropathy((494,495)).”
• The role of advanced glycation end products in progression and complications of diabetes (2008, background): “Furthermore, RAGE knockout mice rendered diabetic have less renal functional and structural injury (27).”