Role of advanced glycation end products in cellular signaling

By Christiane Ott, Kathleen Jacobs, Elisa Haucke, A. Navarrete Santos, T. Grune, A. Simm. Redox Biology, 2014

1,046 citations recorded by the source corpus.

Improvements in health care and lifestyle have led to an elevated lifespan and increased focus on age-associated diseases, such as neurodegeneration, cardiovascular disease, frailty and arteriosclerosis. In all these chronic diseases protein, lipid or nucleic acid modifications are involved, including cross-linked and non-degradable aggregates, such as advanced glycation end products (AGEs). Formation of endogenous or uptake of dietary AGEs can lead to further protein modifications and activation of several inflammatory signaling pathways. This review will give an overview of the most prominent AGE-mediated signaling cascades, AGE receptor interactions, prevention of AGE formation and the impact of AGEs during pathophysiological processes.

Subfields: Clinical Biochemistry, Endocrinology, Diabetes and Metabolism, Nutrition and Dietetics

View Paper: https://www.semanticscholar.org/paper/16fbbd61a50e0b9a4504656aeed18a2e1cd3f33c

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In Endocrinology, Diabetes and Metabolism

1. Qingzheng Kang
2. T. Grune
3. Chunxue Yang
4. A. Höhn
5. Kerstin Nowotny
6. Tobias Jung
7. D. Weber

Citations in the corpus

• Diabetic vascular diseases: molecular mechanisms and therapeutic strategies (2023, background): “Glutamine catabolism produces glutamate that is converted to ornithine404 and aspartate397 and these generated amino acids are also involved in the proliferation of EC.405 EC proliferation is reduced after silencing of asparagine synthetase (ASNS), and supplementation with asparagine and α-ketogluta”
• Redox regulation of FoxO transcription factors (2015, background): “Mitochondrial dysfunction can be the result of a metabolic imbalance, such as in the case of hyperglycemia, which is also linked to glycation of proteins and the formation of advanced glycation end products (AGEs), and fosters other oxidative processes causing elevated ROS formation, including NOX a”
• Advanced Glycation End Products and Oxidative Stress in Type 2 Diabetes Mellitus (2015, background): “It has been shown that cells process other AGE receptors which are able to bind extracellular AGEs and mediate their cellular uptake (reviewed in [67]).”
• Advanced Glycation End-Products (AGEs): Formation, Chemistry, Classification, Receptors, and Diseases Related to AGEs (2022, background): “Hence, it has been postulated that it contributes to raising AGE signaling in the early stage; thus, it was termed AGE-R2 [20,124].”
• Oxidative stress and diabetic retinopathy: Molecular mechanisms, pathogenetic role and therapeutic implications (2020, background): “These carbonyl compounds then undergo complicated chemical rearrangements (oxidations and dehydrations) and crosslink to macromolecules to finally form irreversible and stable AGEs [68].”