Receptor for advanced glycation end-products-mediated inflammation and diabetic vascular complications

Yamamoto, Yasuhiko; Yamamoto, Hiroshi

doi:10.1111/j.2040-1124.2011.00125.x

Cited by 11 publications

(8 citation statements)

References 5 publications

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“…The interaction of AGEs and RAGE also promotes expressions of growth factors, proinflammatory cytokines and chemokines, and adhesion molecules through the mitogen-activated protein kinase (MAPK) pathway, leading to NADPH oxidase-mediated ROS generation and translocation of NF-κB ( 23 , 32 ).…”

Section: Advanced Glycosylation End Products and Receptors In Endothementioning

confidence: 99%

Endothelial Dysfunction in Diabetic Retinopathy

et al. 2020

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Diabetic retinopathy (DR) is a diabetic complication which affects retinal function and results in severe loss of vision and relevant retinal diseases. Retinal vascular dysfunction caused by multifactors, such as advanced glycosylation end products and receptors, pro-inflammatory cytokines and chemokines, proliferator-activated receptor-γ disruption, growth factors, oxidative stress, and microRNA. These factors promote retinal endothelial dysfunction, which results in the development of DR. In this review, we summarize the contributors in the pathophysiology of DR for a better understanding of the molecular and cellular mechanism in the development of DR with a special emphasis on retinal endothelial dysfunction.

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Section: Advanced Glycosylation End Products and Receptors In Endothementioning

confidence: 99%

Endothelial Dysfunction in Diabetic Retinopathy

et al. 2020

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“…RAGE belongs to the immunoglobulin superfamily, and is now known as a member of pattern-recognition receptors (PRRs) and as a proinflammatory device. RAGE recognizes a variety of endogenous and exogenous ligands, including AGE, advanced oxidation protein products, high-mobility group box protein 1 (HMGB1), calcium-binding S100 proteins, β2-integrin Mac-1/CD11b, amyloid β peptide/fibril, lipopolysaccharide (LPS), phosphatidylserine, C1q, and lysophosphatidic acid (LPA) (5). It has been hypothesized that RAGE engagement of such ligands causes diabetic vascular complications, atherosclerosis, cancer, neurodegeneration, and inflammatory diseases (6).…”

Section: Innate Immunity and Rage-mediated Inflammatory Reactionsmentioning

confidence: 99%

RAGE-Mediated Inflammation, Type 2 Diabetes, and Diabetic Vascular Complication

Yamamoto¹,

Yamamoto²

2013

Front. Endocrinol.

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Obesity is associated with inflammation and type 2 diabetes. Innate immune system comprised of cellular and molecular components plays an important role in the inflammatory reactions. Immune cells like macrophages and their cell surface pattern-recognition receptors (PRRs) are representative for innate immunity promoting inflammatory reactions. The receptor for advanced glycation end-products (RAGE) is a member of PRRs and a proinflammatory molecular device that mediates danger signals to the body. The expression of RAGE is observed in adipocytes as well as immune cells, endothelial cells, and pancreatic β cells under certain conditions. It has been reported that RAGE is implicated in adipocyte hypertrophy and insulin resistance. RAGE-mediated regulation of adiposity and inflammation may attribute to type 2 diabetes and diabetic vascular complications.

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“…Of them, our group and others focus on the glycation reaction and advanced glycation end-products (AGE) implicated in the pathogenesis of diabetic nephropathy [5, 6]. The receptor for AGE (RAGE) association with ligands triggers the acceleration of this disease [7]. For example, RAGE-overexpressing diabetic mice showed progressive glomerulosclerosis with renal dysfunction, compared to diabetic littermates lacking the RAGE transgene [8].…”

Section: Introductionmentioning

confidence: 99%

Preventive Effect of Salicylate and Pyridoxamine on Diabetic Nephropathy

Abouzed

Harashima

Masuo

et al. 2016

Journal of Diabetes Research

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Objective. Diabetic nephropathy is a life-threatening complication in patients with long-standing diabetes. Hemodynamic, inflammatory, and metabolic factors are considered as developmental factors for diabetic nephropathy. In this study, we evaluated whether pharmacological interventions with salicylate, compared to pyridoxamine, could prevent diabetic nephropathy in mice. Methods. Male mice overexpressing inducible nitric oxide synthase in pancreatic β-cells were employed as a diabetic model. Salicylate (3 g/kg diet) or pyridoxamine (1 g/L drinking water; ~200 mg/kg/day) was given for 16 weeks to assess the development of diabetic nephropathy. Treatment with long-acting insulin (Levemir 2 units/kg twice a day) was used as a control. Results. Although higher blood glucose levels were not significantly affected by pyridoxamine, early to late stage indices of nephropathy were attenuated, including kidney enlargement, albuminuria, and increased serum creatinine, glomerulosclerosis, and inflammatory and profibrotic gene expressions. Salicylate showed beneficial effects on diabetic nephropathy similar to those of pyridoxamine, which include lowering blood glucose levels and inhibiting macrophage infiltration into the kidneys. Attenuation of macrophage infiltration into the kidneys and upregulation of antiglycating enzyme glyoxalase 1 gene expression were found only in the salicylate treatment group. Conclusions. Treatment with salicylate and pyridoxamine could prevent the development of diabetic nephropathy in mice and, therefore, would be a potentially useful therapeutic strategy against kidney problems in patients with diabetes.

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Receptor for advanced glycation end-products-mediated inflammation and diabetic vascular complications

Cited by 11 publications

References 5 publications

Endothelial Dysfunction in Diabetic Retinopathy

Endothelial Dysfunction in Diabetic Retinopathy

RAGE-Mediated Inflammation, Type 2 Diabetes, and Diabetic Vascular Complication

Preventive Effect of Salicylate and Pyridoxamine on Diabetic Nephropathy

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