Advanced Glycation End Products in Aging and Age-Related Diseases

Dear Colleagues,

Advanced glycation end products (AGEs) have long been considered as potently toxic molecules that promote host cell death, contributing to organ damage in living animals, including humans. AGEs can induce the development and progression of diabetic complications and many other diseases, including cardiovascular diseases and neurodegenerative diseases such as Alzheimer's disease, Parkinson’s disease, and alcoholic brain damage.

AGEs represent a heterogeneous group of irreversible products resulting from the non-enzymatic glycation and oxidation of proteins, nucleic acids, and lipids. AGEs bind with their receptor RAGE (receptor for advanced glycation end products), which is highly upregulated during host cell death through reactive oxygen species (ROS) and strong activations of the extracellular signal-regulated kinase 1/2 (ERK1/2) and nuclear factor kappa B (NF-κB) pathways in many diseases. The inhibition of AGEs in blood or activated macrophages has been positively correlated with the decreased pathogenesis of several diseases.

Glycation produces AGE compounds with toxic properties associated with inflammation and oxidative stress. AGEs accumulate in the extracellular matrix of various tissues, and significantly contribute to the development of various chronic diseases in many organs. Furthermore, AGEs have been shown to become antigenic, and thus, to induce immune responses. AGEs also exhibit adverse effects on cellular functions by cross-linking intracellular and extracellular proteins, which trigger diverse diseases. Therefore, several agents (e.g., anti-inflammatory molecules) have been developed to ameliorate their adverse effects.

This Special Issue of Biomolecules aims to include several original reports and review articles focused on the molecular mechanisms of organ damage through post-translational protein modifications; alterations of the cellular signaling pathways; the promotion of ER stress; mitochondrial dysfunction and the apoptosis of cells/tissues; as well as translational research of biomarker discovery, prevention, and potential therapy.

Prof. Bonghee Lee
Dr. Byoung Joon Song
Guest Editors

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• oxidative stress
• post-translational protein modifications
• apoptosis of cells/tissues
• aging-related diseases
• biomarker discovery
• prevention and therapy