Glycation in Health and Disease
A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Chemical Biology".
Deadline for manuscript submissions: closed (15 March 2023) | Viewed by 2317
Special Issue Editors
Interests: glycation biology; mitochondrial perturbation; neurodegeneratisson; metabolic disorders; cell and molecular biology
Interests: medical biotechnology; genetics and molecular medicine
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Glycation is the result of the covalent bonding of a free amino group from a biological macromolecule (DNA, protein & lipids) to reduced sugars or dicarbonyls, which results in the formation of advanced glycation end products (AGEs). Glycation has gained substantial attention recently for its alleged influence over various diseases’ progression such as diabetes, atherosclerosis, cancer, and Alzheimer’s disease. Age-related accumulation of AGEs could serve as danger signals to initiate and accelerate disease processes via mitochondrial perturbation. Glycation can trigger variable transcription factors, such as nuclear factor erythroid-2-related factor (Nrf2), nuclear factor kappa B (NF-κB), protein-53 (p-53), activating protein-1 (AP-1), hypoxia-inducible factor-1α (HIF-1α), β-catenin/Wnt, and peroxisome proliferator-activated receptor-γ (PPAR-γ). Activated transcription factors can lead to approximately 500 different alterations in gene expression and can alter the expression patterns of inflammatory cytokines, growth factors, regulatory cell cycle molecules, and anti-inflammatory molecules. In addition, the receptor of AGE (RAGE) has been linked to various signaling pathways such as extracellular signal‑regulated protein kinase ½ (ERK1/2), c-Jun N-terminal Kinase (JNK), and p38 mitogen-activated protein kinase (MAPK). In addition, evidence suggests that glycoxidative stress can cause epigenetic chromatin changes in target cells by activating signaling pathways that regulate epigenetic factors, resulting in dysregulated expression of vital genes. Furthermore, how these pathways, transcription factors, and epigenetic alterations are conveyed through numerous pathologies’ progression is still not fully understood. Our proposed work is expected to greatly enhance our understanding of glycation states under health and disease conditions. Published data and explanations will no doubt accelerate the discovery of new therapeutic targets for the treatment of glycation-associated complications in relation to health and disease.
Dr. Firoz Akhter
Dr. Khurshid Ahmad
Guest Editors
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Keywords
- biological macromolecules
- AGEs
- RAGE
- mitochondrial perturbation
- glycoxidative stress
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