RAGE drives the development of glomerulosclerosis and implicates podocyte activation in the pathogenesis of diabetic nephropathy. - Wikidata - wikimedia - TriplyDB

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

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

http://www.wikidata.org/entity/Q42263637

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Receptor for advanced glycation end products and its involvement in inflammatory diseases Circulating HMGB1 and RAGE as Clinical Biomarkers in Malignant and Autoimmune Diseases Role of Neuropilin-1 in Diabetic Nephropathy Molecular mechanisms of diabetic kidney disease The -374 T/A polymorphism in the gene encoding RAGE is associated with diabetic nephropathy and retinopathy in type 1 diabetic patients RAGE and CYBA polymorphisms are associated with microalbuminuria and end-stage renal disease onset in a cohort of type 1 diabetes mellitus patients over a 20-year follow-up A role for the receptor for advanced glycation end products in idiopathic pulmonary fibrosis cAMP ameliorates inflammation by modulation of macrophage receptor for advanced glycation end-products The multiple faces of RAGE--opportunities for therapeutic intervention in aging and chronic disease Microglial receptor for advanced glycation end product-dependent signal pathway drives beta-amyloid-induced synaptic depression and long-term depression impairment in entorhinal cortex.Dangers within: DAMP responses to damage and cell death in kidney disease.The sour side of neurodegenerative disorders: the effects of protein glycation.Podocyte-selective deletion of dicer induces proteinuria and glomerulosclerosis.Molecular mechanisms of diabetic vascular complications Controlling the receptor for advanced glycation end-products to conquer diabetic vascular complications RAGE gene deletion inhibits the development and progression of ductal neoplasia and prolongs survival in a murine model of pancreatic cancer.The glomerulus--a view from the outside--the podocyte.Higher plasma soluble Receptor for Advanced Glycation End Products (sRAGE) levels are associated with incident cardiovascular disease and all-cause mortality in type 1 diabetes: a 12-year follow-up study.Deletion of the receptor for advanced glycation end products reduces glomerulosclerosis and preserves renal function in the diabetic OVE26 mouse.Soluble RAGE: therapy and biomarker in unraveling the RAGE axis in chronic disease and aging Local and systemic RAGE axis changes in pulmonary hypertension: CTEPH and iPAH Obesity in kidney disease: A heavyweight opponent.C-peptide and diabetic kidney disease.Modulation of the cellular expression of circulating advanced glycation end-product receptors in type 2 diabetic nephropathy.Promoting effects of the adipokine, apelin, on diabetic nephropathy.-374 T/A RAGE polymorphism is associated with chronic kidney disease progression in subjects affected by nephrocardiovascular disease.Paradoxical function for the receptor for advanced glycation end products in mouse models of pulmonary fibrosis.Messenger RNA levels of podocyte-associated proteins in subjects with different degrees of glucose tolerance with or without nephropathy Alternative splicing of the RAGE cytoplasmic domain regulates cell signaling and function.RAGE signaling significantly impacts tumorigenesis and hepatic tumor growth in murine models of colorectal carcinoma.New insight into the molecular drug target of diabetic nephropathy.Regulation of RAGE for attenuating progression of diabetic vascular complications.Growth factors and the development of diabetic nephropathy.Mechanisms and consequences of TGF-ß overexpression by podocytes in progressive podocyte disease.Use of genetic mouse models in the study of diabetic nephropathy.Sesamin Ameliorates Advanced Glycation End Products-Induced Pancreatic β-Cell Dysfunction and Apoptosis.Early- and advanced non-enzymatic glycation in diabetic vascular complications: the search for therapeutics.Antiproteinuric effect of RAS blockade: new mechanisms.Role of advanced glycation end products in cardiovascular disease.RAGE and TGF-β1 Cross-Talk Regulate Extracellular Matrix Turnover and Cytokine Synthesis in AGEs Exposed Fibroblast Cells

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

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Bernd Arnold

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P2860

RAGE mediates a novel proinflammatory axis: a central cell surface receptor for S100/calgranulin polypeptides

Cloning and expression of a cell surface receptor for advanced glycosylation end products of proteins

Migration of human monocytes in response to vascular endothelial growth factor (VEGF) is mediated via the VEGF receptor flt-1

Transforming growth factor beta in tissue fibrosis

The S100 family of EF-hand calcium-binding proteins: functions and pathology

The S100 protein family: history, function, and expression

Development and prevention of advanced diabetic nephropathy in RAGE-overexpressing mice

Advanced glycation end products cause epithelial-myofibroblast transdifferentiation via the receptor for advanced glycation end products (RAGE)

N(epsilon)-(carboxymethyl)lysine adducts of proteins are ligands for receptor for advanced glycation end products that activate cell signaling pathways and modulate gene expression

Progression of diabetic nephropathy. Insights from cell culture studies and animal models.

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