Advanced Glycation End Products in Aging and Age-Related Diseases

A special issue of Biomolecules (ISSN 2218-273X).

Deadline for manuscript submissions: closed (30 April 2020) | Viewed by 364

Special Issue Editors


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Guest Editor
Center for Genomics and Proteomics, School of Medicine, Gachon University, Incheon 406-840, Republic of Korea
Interests: stem cell CRISPR editing; stem cell therapeutics; allogeneic manufacturing; CAR-T/NK cells; stem cell proteomics/genomics
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Chief, Section of Molecular Pharmacology and Toxicology Laboratory of Membrane Biochemistry and Biophysics, National Institute on Alcohol Abuse and Alcoholism, 5625 Fishers Lane, Room 3N-01, Rockville, MD, USA
Interests: CYP2E1; oxidative stress; post-translational protein modifications; ER stress; mitochondrial dysfunction; JNK-mediated apoptosis signaling; tissue injury via the gut-liver-brain axis; exosomes; alcohol and nonalcoholic substances
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

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

Manuscript Submission Information

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Keywords

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

Published Papers

There is no accepted submissions to this special issue at this moment.
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