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 2090

Special Issue Editors


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Guest Editor
Department of Biomedical Engineering, Stony Brook University, New York, NY 11794-5281, USA
Interests: glycation biology; mitochondrial perturbation; neurodegeneratisson; metabolic disorders; cell and molecular biology

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Co-Guest Editor
Department of Medical Biotechnology, Yeungnam University, Gyeongsan 38541, Republic of Korea
Interests: bioinformatics; extracellular matrix biology; muscle biology; drug designing; virtual screening
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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

Published Papers (1 paper)

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Research

11 pages, 768 KiB  
Article
Concentrations of N6-Carboxymethyllysine (CML), N6-Carboxyethyllysine (CEL), and Soluble Receptor for Advanced Glycation End-Products (sRAGE) Are Increased in Psoriatic Patients
by Aleksandra Damasiewicz-Bodzek and Agnieszka Nowak
Biomolecules 2022, 12(12), 1870; https://doi.org/10.3390/biom12121870 - 13 Dec 2022
Cited by 1 | Viewed by 1259
Abstract
Psoriasis is a chronic, recurrent, and often severe skin disease which is frequently associated with metabolic disorders and increased risk of cardiovascular complications. One of the postulated links is an intensified process of advanced protein glycation and/or glycoxidation. Therefore, the aim of the [...] Read more.
Psoriasis is a chronic, recurrent, and often severe skin disease which is frequently associated with metabolic disorders and increased risk of cardiovascular complications. One of the postulated links is an intensified process of advanced protein glycation and/or glycoxidation. Therefore, the aim of the study was to assess concentrations of N6-carboxymethyllysine (CML), N6-carboxyethyllysine (CEL), and soluble form of receptor for advanced glycation end-products (sRAGE) in psoriasis patients at different phases of the disease activity, in comparison to healthy individuals. The study material consisted of sera from psoriasis patients in active phase, in the remission phase, and healthy controls. Concentrations of CML, CEL, and sRAGE were determined using ELISA technique. In the patients with psoriasis (in both phases of the disease), concentrations of CML, CEL and sRAGE were significantly higher than in healthy individuals but they did not correlate with psoriasis area severity index (PASI) values. The remission of the disease was followed by a significant decrease in CML, CEL, and sRAGE concentrations when compared to active patients; however, these concentrations were still significantly higher than in the controls. Our data suggest that psoriasis is accompanied by an intense glycoxidation process and that high sRAGE levels seem to reflect permanent RAGE overstimulation. Full article
(This article belongs to the Special Issue Glycation in Health and Disease)
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