Results 171 to 180 of about 87,091 (210)
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Advanced glycation end products and the kidney
American Journal of Physiology-Renal Physiology, 2005Advanced glycation end products (AGEs) are a heterogeneous group of protein and lipids to which sugar residues are covalently bound. AGE formation is increased in situations with hyperglycemia (e.g., diabetes mellitus) and is also stimulated by oxidative stress, for example in uremia.
Jürgen M, Bohlender +3 more
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Methods to assess advanced glycation end-products
Current Opinion in Clinical Nutrition & Metabolic Care, 2021Purpose of review Advanced glycation end-products (AGEs) resulting from protein glycoxidation constitute biomarkers of interest in different pathological situations. Several methods for quantifying AGEs in biological fluids or tissues have been developed without any real consensus on a gold standard method.
Stéphane, Jaisson, Philippe, Gillery
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Advanced glycation and glycoxidation end products in bone
Bone, 2023Hyperglycemia and oxidative stress, enhanced in diabetes and aging, result in excessive accumulation of advanced glycation and glycoxidation end products (AGEs/AGOEs) in bone. AGEs/AGOES are considered to be "the missing link" in explaining increased skeletal fragility with diabetes, aging, and osteoporosis where increased fracture risk cannot be ...
Bowen, Wang, Deepak, Vashishth
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Advanced Glycation End Products and Diabetic Nephropathy
American Journal of Therapeutics, 2005Chronic hyperglycemia and oxidative stress in diabetes results in the formation and accumulation advanced glycation end products (AGEs). AGEs have a wide range of chemical, cellular, and tissue effects that contribute to the development of microvascular complications. In particular, AGEs appear to have a key role in the diabetic nephropathy.
Thomas, Merlin C. +2 more
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Advanced glycation end products: A nephrologist's perspective
American Journal of Kidney Diseases, 2000Advanced glycation end products (AGEs) are a heterogeneous group of molecules that accumulate in plasma and tissues with advancing age, diabetes, and renal failure. There is emerging evidence that AGEs are potential uremic toxins and may have a role in the pathogenesis of vascular and renal complications associated with diabetes and aging.
D S, Raj +3 more
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Advanced Glycation End Products
2020Advanced glycation end products (AGEs) play a major role in diabetic vascular complications, such as chronic kidney disease (CKD), by activating pro-oxidant and pro-inflammatory responses. Although traditionally AGEs have been associated with uncontrolled hyperglycemia of diabetes mellitus, there is increasing evidence that exogenous AGEs from diet ...
Annabel Biruete, Jaime Uribarri
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Advanced Glycation End Products and Insulin Resistance
Current Pharmaceutical Design, 2008Non-enzymatic modification of proteins by reducing sugars, a process that is also known as Maillard reaction, leads to the formation of advanced glycation end products (AGEs) in vivo. There is a growing body of evidence that formation and accumulation of AGEs progress during normal aging, and at an extremely accelerated rate under diabetes, thus being ...
Hiroyuki, Unoki, Sho-ichi, Yamagishi
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Advanced Glycation End Products and Diabetic Retinopathy
Current Medicinal Chemistry, 2013Diabetic retinopathy (DR) has a complex pathogenesis which is impacted by a raft of systemic abnormalities and tissue-specific alterations occurring in response to the diabetes milieu. Many pathogenic processes play key roles in retinal damage in diabetic patients.
Chen, M., Curtis, T. M., Stitt, A. W.
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Advanced Glycation End Products
2011Prolonged hyperglycemia, dyslipidemia and oxidative stress in diabetes result in the increased production and accumulation of advanced glycation end products (AGEs) in the kidney. Covalent AGE modifications significantly influence the structure and function of key protein targets.
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Advanced glycation end products and diabetic retinopathy
Amino Acids, 2011Retinopathy is a serious microvascular complication of diabetes and a major cause of blindness in young adults, worldwide. Early diabetic retinopathy is characterized by a loss of pericytes from retinal capillaries, the appearance of acellular capillaries and microaneurysms, and a breakdown of the blood-retinal barrier. In later stages, this can evolve
Ross, Milne, Seymour, Brownstein
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