Advanced glycation end-products: a review
By R. Singh, A. Barden, T. A. Mori, L. Beilin. Diabetologia, 2001
2,544 citations recorded by the source corpus.
Subfields: Clinical Biochemistry, Endocrinology, Diabetes and Metabolism, Neurology
View Paper: https://www.semanticscholar.org/paper/f90981b343df2266c5264af7e4002d5f262b6dda
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In Clinical Biochemistry
In Endocrinology, Diabetes and Metabolism
In Neurology
Citations in the corpus
- Treatment of NAFLD with diet, physical activity and exercise. (2017, background): “AGEs are related to the aetiology of diabetes and other metabolic alterations.(34,37,38) They have been shown to be elevated in NASH patients compared to simple steatosis and controls, and to be positively correlated with insulin resistance and negatively with adiponectin.”
- Aldehyde Sources, Metabolism, Molecular Toxicity Mechanisms, and Possible Effects on Human Health (2005, background): “…protein glycoxidation or lipoxidation leading to tissue deterioration also occured in several pathological conditions other than diabetes toxicity (Singh et al., 2001b), such as cardiovascular diseases including atherosclerosis (Baynes et al., 2000; Uchida, 2000) and uremia (Miyata et al., 2001),…”
- Advanced Glycation End Products and Diabetes Mellitus: Mechanisms and Perspectives (2022, background): “AGEs constitute a complex heterogeneous group of compounds that can be produced endogenously or taken up as dietary AGEs [18,27].”
- The role of oxidative stress in diabetic complications (2007, background): “The Schiff base is then reduced to an Amadori product and subsequent oxidations and crosslinking occur, yielding a diverse group of modifications referred to as AGE (275,276).”
- Role of advanced glycation end products in cellular signaling (2014, background): “The combination of increased blood glucose, oxidative and non-oxidative processes result in rearrangements of the Amadori products into the irreversible advanced glycation end products [3,17].”
- Advanced Glycation End Products and Oxidative Stress in Type 2 Diabetes Mellitus (2015, background): “Formation of reactive dicarbonyls and AGEs, modified according to [29].”
- Pathogenesis of Diabetic Nephropathy (2004, positive): “This process is further enhanced by monocyte chemotaxis, adhesion-molecule expression, decreased prostacycline formation and plasminogenactivator inhibitor-1 (PAI-1) induction [ 57 ].”
- Advanced Glycation End-Products (AGEs): Formation, Chemistry, Classification, Receptors, and Diseases Related to AGEs (2022, background): “Among these, so far, the best-characterized are pentosidine and CML [37].”