A5030113532- Advanced Glycation End Products research
- Natural Antidiabetic Agents Studies
- Diabetes, Cardiovascular Risks, and Lipoproteins
- Chronic Kidney Disease and Diabetes
- Retinal Diseases and Treatments
- Diabetes Treatment and Management
- Alcohol Consumption and Health Effects
- Atherosclerosis and Cardiovascular Diseases
- Neurological Disorders and Treatments
- Neurological Disease Mechanisms and Treatments
- Liver Disease Diagnosis and Treatment
- Peroxisome Proliferator-Activated Receptors
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Renin-Angiotensin System Studies
- Nitric Oxide and Endothelin Effects
- Cardiovascular Health and Disease Prevention
- Diet, Metabolism, and Disease
- Pancreatic function and diabetes
- Blood Pressure and Hypertension Studies
- Antiplatelet Therapy and Cardiovascular Diseases
- Diabetes Management and Research
- Eicosanoids and Hypertension Pharmacology
- Adipokines, Inflammation, and Metabolic Diseases
- Cardiovascular Disease and Adiposity
- Acute Ischemic Stroke Management
Showa University
2019-2025
Kurume University
2010-2019
University School
2010-2019
Icahn School of Medicine at Mount Sinai
2016
Yokohama City University Medical Center
2014
Yokohama City University
2014
Kanagawa Cardiovascular and Respiratory Center
2014
Teikyo University
2014
Hiroshima University
2008-2014
Yokohama Sakae Kyosai Hospital
2014
The binding of advanced glycation end products (AGE) to the receptor for AGE (RAGE) is known deteriorate various cell functions and implicated in pathogenesis diabetic vascular complications. Here we show that AGE, tumor necrosis factor-α (TNF-α), 17β-estradiol (E2) up-regulated RAGE mRNA protein levels human microvascular endothelial cells ECV304 cells, with stability being essentially invariant. Transient transfection experiments promoter-luciferase chimeras revealed region from nucleotide...
Advanced glycation end products (AGEs) and receptor RAGE play a role in diabetic nephropathy. We have previously shown that increased glucose uptake into proximal tubular cells via sodium-glucose cotransporter 2 (SGLT2) stimulates oxidative stress generation expression, thereby exacerbating the AGE-induced apoptosis this cell type. However, protective of SGLT2 inhibition against AGE-RAGE-induced renal damage animals remains unclear. In study, we investigated effects empagliflozin, inhibitor...
Advanced glycation end products (AGE) have been implicated in the pathogenesis of glomerulosclerosis diabetes. However, their involvement development early phase diabetic nephropathy has not fully elucidated. We investigated effects AGE on growth and vascular endothelial factor (VEGF) monocyte chemoattractant protein-1 (MCP-1) expression human cultured mesangial cells. prepared three immunochemically distinct by incubating bovine serum albumin (BSA) with glucose, glyceraldehyde, or...
Hypoxia is the principal factor that causes angiogenesis. These experiments were conducted to explore how it induces proliferation of vascular cells, a key step in Human umbilical vein endothelial cells and bovine retinal pericytes grown controlled atmosphere culture chambers containing various concentrations oxygen. The numbers both increased significantly under hypoxic conditions; O2 achieved maximal growth promotion 10% for 2.5% pericytes. Quantitative reverse transcription-polymerase...
The impact of AGEs on human MSCs was studied. inhibited the proliferation MSCs, induced apoptosis, and prevented cognate differentiation into adipose tissue, cartilage, bone, suggesting a deleterious effect in pathogenesis musculoskeletal disorders aged diabetic patients.Advanced glycation end-products (AGEs) are accumulated long-lived proteins various tissues advanced age diabetes mellitus have been implicated chronic complication, including disorders. Human mesenchymal stem cells (MSCs)...
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 diabetic microangiopathy. We first prepared AGE-bovine serum albumin (BSA) anti-AGE antiserum using AGE-RNase A. Then AGE-BSA administered human skin microvascular endothelial cells culture, their growth examined. The AGE-BSA, but not nonglycated BSA, found induce...
We previously have found that advanced glycation end products (AGE), senescent macroproteins formed at an accelerated rate in diabetes, arise vivo not only from glucose but also reducing sugars. Furthermore, we recently shown glyceraldehyde- and glycolaldehyde-derived AGE (glycer- glycol-AGE) are mainly involved loss of pericytes, the earliest histopathological hallmark diabetic retinopathy. However, effects these proteins on angiogenesis, another vascular derangement retinopathy, remain to...
The transcription factor Nrf2 regulates the expression of antioxidant genes. Hyperglycemia-induced oxidative stress is involved in pathogenesis diabetes and its complications. However, little known about protective role diabetes. To gain insight into we treated knockout (Nrf2 KO) mice with streptozotocin (STZ). STZ KO did not develop renal hyperfiltration, which was observed STZ-treated wild-type (STZ WT) mice, but function gradually deteriorated over 10-week observation period. Urinary...
Pigment epithelium-derived factor (PEDF), a potent inhibitor of angiogenesis with neuronal differentiating activity, inhibits endothelial cell injury in vitro, thus suggesting the involvement PEDF atherosclerosis. Therefore, elucidating relationship between serum levels and coronary risk factors could provide clue to understanding pathophysiological role vivo.We examined whether were associated for artery disease.The study was designed as cross-sectional study.The set within general...