Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy
By H. Hammes, Xueliang Du, D. Edelstein, T. Taguchi, T. Matsumura, Qida Ju, Ji-hong Lin, A. Bierhaus, P. Nawroth, D. Hannak and 4 more. Nature Medicine, 2003
816 citations recorded by the source corpus.
Subfields: Biochemistry, Neurology, Pathology and Forensic Medicine
View Paper: https://www.semanticscholar.org/paper/28c9d44b998b0654312f6efd9075a5f2f98ab079
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Citations in the corpus
- The role of advanced glycation end products in progression and complications of diabetes (2008, background): “Benfotiamine, a lipid-soluble thiamine (vitamin B1) derivative, prevents activation of three major pathways of hyperglycemic damage (hexosamine pathway, intracellular AGE formation, and the diacylglycerol-protein kinase C pathway) by increasing the activity of transketolase, the rate-limiting enzyme”
- Molecular basis of the inner blood-retinal barrier and its breakdown in diabetic macular edema and other pathological conditions. (2013, background): “apoptosis of retinal endothelial cells (Brownlee, 2005; Hammes et al., 2003).”
- Dietary factors and low-grade inflammation in relation to overweight and obesity (2011, positive): “Likewise, the preventive effect of benfotiamine, a transketolase activator that directs glucose substrates to the pentose phosphate pathway, might depend on the consequent blockade of endogenous dicarbonyls and AGE formation as well as of other hyperglycaemia-induced pathways((536)).”
- Contributions of Inflammatory Processes to the Development of the Early Stages of Diabetic Retinopathy (2007, background): “In addition, administration of benfotiamine significantly inhibited the development of acellular capillaries in retinas of diabetic rats [137].”
- Inhibition of GAPDH activity by poly(ADP-ribose) polymerase activates three major pathways of hyperglycemic damage in endothelial cells. (2003, background): “This epitope was chosen because methylglyoxal is the principal AGE precursor induced in endothelial cells by hyperglycemia (18, 19), and the hydroimidazolone adduct is the major methylglyoxalderived epitope (18).”
- Mechanisms of diabetic complications. (2013, background): “Moreover, diabetes-induced increases in NF- B activation are prevented by numerous therapeutics including metformin (270), aspirin (683), vitamin B derivatives (232), carnosine (436), and thiazolidinediones (370).”
- Oxidative Stress and Diabetic Retinopathy (2007, background): “Benfotiamine, a lipid soluble thiamine (vitamin B1) derivative that inhibits MnSOD, has been shown to inhibit increases in acellular capillaries in the retina of diabetic rats via blocking the major pathways involved in hyperglycemiainduced retinal dysmetabolism, including AGEs, PKC, and hexosamine ”
- Oxidative stress and diabetic retinopathy: Molecular mechanisms, pathogenetic role and therapeutic implications (2020, background): “blockage of three major biochemical pathways – the hexosamine/AGE formation/PKC Pathway, which finally suppresses the development of DR [265].”
- The pathobiology of diabetic complications: a unifying mechanism. (2005, background): “Most importantly, benfotiamine treatment completely prevented the major structural lesion of both human nonproliferative retinopathy and experimental diabetic retinopathy: acellular capillaries (50).”
- Advanced glycation end products and RAGE: a common thread in aging, diabetes, neurodegeneration, and inflammation. (2005, background): “Signaling cascades activated upon ligand–RAGE interaction include pathways such as p21ras, erk1/2 (p44/p42) MAP kinases, p38 and SAPK/JNK MAP kinases, rho GTPases, phosphoinositol-3 kinase, and the JAK/STAT pathway; downstream consequences such as the activation of the key transcription factors, NF-”