Recent experimental findings suggest that free oxygen radicals and AGEs may be significantly involved in the onset and development of chronic diabetic complications and Alzheimer's disease. The presented review summarizes knowledge on structure and rise of these products in vitro and in vivo and the chemical and biological properties of advanced glycation endproducts are discussed. Strategy of influencing development and prevention of diabetic complications in the near future involves a potentially promising antiglycation therapy and supplementation by antioxidants.
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Clin Neuroradiol
January 2025
Department of Endocrinology, Diabetology, Metabolic Diseases and Clinical Chemistry (Internal Medicine 1), Heidelberg University Hospital, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
Background: Cardiovascular risk management is beneficial, but stringent glycemic control does not prevent the progression of distal sensorimotor polyneuropathy (DSPN). Persistent hyperglycemia-induced alterations and cardiovascular factors may contribute to diabetes-associated nerve damage. This study aimed to evaluate the correlation between skin auto-fluorescence (sAF), an indicator of dermal advanced glycation end-product (AGE) accumulations, cardiovascular risk, and changes in peripheral nerve integrity.
View Article and Find Full Text PDFSci Transl Med
January 2025
Department of Surgery, UT Southwestern Medical Center, Dallas, TX 75390, USA.
Pancreatic ductal adenocarcinoma (PDAC) driven by the mutation presents a formidable health challenge because of limited treatment options. MRTX1133 is a highly selective and first-in-class KRAS-G12D inhibitor under clinical development. Here, we report that the advanced glycosylation end product-specific receptor (AGER) plays a key role in mediating MRTX1133 resistance in PDAC cells.
View Article and Find Full Text PDFFront Cardiovasc Med
January 2025
School of Life Sciences, Beijing University of Chinese Medicine, Beijing, China.
Cardiometabolic diseases (CMD) are leading causes of death and disability worldwide, with complex pathophysiological mechanisms in which inflammation plays a crucial role. This review aims to elucidate the molecular and cellular mechanisms within the inflammatory microenvironment of atherosclerosis, hypertension and diabetic cardiomyopathy. In atherosclerosis, oxidized low-density lipoprotein (ox-LDL) and pro-inflammatory cytokines such as Interleukin-6 (IL-6) and Tumor Necrosis Factor-alpha (TNF-α) activate immune cells contributing to foam cell formation and arterial wall thickening.
View Article and Find Full Text PDFJPEN J Parenter Enteral Nutr
January 2025
The University of Queensland, Brisbane, Australia.
Background: Advanced glycation end-products (AGEs) can enter patients' circulation through exogenous sources, such as enteral nutrition formulae. Circulating AGEs, specifically carboxymethyllysine, can promote insulin resistance and activation of pro-inflammatory pathways leading to oxidative stress, cell death, and organ failure. Suboptimal kidney function increases the risk of elevated circulating AGEs because levels are controlled through urinary excretion.
View Article and Find Full Text PDFMol Cell Endocrinol
January 2025
Division of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, Albert Einstein College of Medicine/Montefiore Medical Center, Bronx, NY, USA; Reproductive Medicine Associates of New York, Department of Obstetrics, Gynecology and Reproductive Science, Division of Reproductive Endocrinology and Infertility, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
The purpose of this study was to examine the deposition of advanced glycation end products (AGEs) and their receptors, RAGE, in ovarian follicles during folliculogenesis in mice fed high (H-AGE) or low (L-AGE) AGE diets and following superovulation with gonadotropins. We hypothesize that H-AGE diet is associated with increased AGE deposition and RAGE expression in various stages of ovarian follicular development, and superovulation with gonadotropins may alter these changes. C57BL/6J mice were fed low L-AGE (n=10) or H-AGE (n=10) diet for 12 weeks.
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