Results 21 to 30 of about 46,188 (214)
Dietary Advanced Glycation End Products and Aging [PDF]
Advanced glycation end products (AGEs) are a heterogeneous, complex group of compounds that are formed when reducing sugar reacts in a non-enzymatic way with amino acids in proteins and other macromolecules. This occurs both exogenously (in food) and endogenously (in humans) with greater concentrations found in older adults.
Luevano-Contreras, Claudia +1 more
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Advanced Glycation End-products and Atherosclerosis
The late rearrangements of the covalent nonenzymatic modification of proteins by glucose, called advanced glycation end-products (AGEs), have been shown to accumulate in diabetic and ageing tissues. AGEs elicit a wide range of cell-mediated responses leading to vascular dysfunction, matrix expansion and athero- and glomerulosclerosis.
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Advanced Glycation End Products in Clinical Nephrology
As a result of oxidative and carbonyl stress, advanced glycation end products (AGEs) are involved in the pathogenesis of severe and frequent diseases and their fatal vascular/cardiovascular complications, i.e. diabetes mellitus and its complications (nephropathy, angiopathy, neuropathy and retinopathy, renal failure and uremic and dialysis-associated ...
M, Kalousová +4 more
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Toxicity of advanced glycation end products (Review)
Advanced glycation end-products (AGEs) are proteins or lipids glycated nonenzymatically by glucose, or other reducing sugars and their derivatives, such as glyceraldehyde, glycolaldehyde, methyloglyoxal and acetaldehyde. There are three different means of AGE formation: i) Maillard reactions, the polyol pathway and lipid peroxidation.
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Advanced glycation end products and diabetic retinopathy [PDF]
Studies have established hyperglycemia as the most important factor in the progress of vascular complications. Formation of advanced glycation end products (AGEs) correlates with glycemic control. The AGE hypothesis proposes that hyperglycemia contributes to the pathogenesis of diabetic complications including retinopathy.
Yashodhara, Sharma +4 more
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An AuNPs/fMWCNT nanocomposite‐modified screen‐printed carbon electrode was engineered via sequential electrodeposition and integrated into a 3D‐printed microfluidic platform for ultrasensitive methylglyoxal detection. The non‐invasive sensing platform enables rapid analysis in saliva and sweat, highlighting strong potential for wearable point‐of‐care ...
Ahadul Amin Soshi +3 more
wiley +1 more source
This project developed a smart bandage‐like patch (a microneedle array) for repairing diabetic bone damage. It intelligently senses signals from infection and inflammation, then releases its medicines in a specific, timed sequence: first an antibacterial agent, then an anti‐inflammatory agent, and finally growth factors.
Yu Wang +10 more
wiley +1 more source
Malectin alleviates high glucose‐induced ER stress and damage in placental trophoblasts, a function dependent on its six critical carbohydrate‐binding residues. In a GDM mouse model, administration of TAT‐Malectin ameliorated hyperglycemia and placental ER stress and prevented fetal macrosomia.
Jiahui Zhu +12 more
wiley +1 more source
ABSTRACT Advancements in tissue engineering have revolutionized therapeutic paradigms for diabetic tissue defects; however, the lack of applicable scaffold containing various bioactive substance aggregates remained a critical bottleneck hindering satisfactory repair effect.
Tao Wang +8 more
wiley +1 more source
This study identifies that methylglyoxal may play an important role in heart‐brain interactions after myocardial infarction. Myocardial infarction leads to increased levels of methylglyoxal‐derived advanced glycation end‐products (MG‐H1) in the brain of mice, which is associated with loss of blood‐brain barrier integrity and neuroinflammation ...
Ramis Ileri, Xixi Guo, Erik J. Suuronen
wiley +1 more source

