Methylglyoxal-Derived Advanced Glycation Endproducts in Multiple Sclerosis

Multiple sclerosis (MS) is a demyelinating disease of the central nervous system (CNS). The activation of inflammatory cells is crucial for the development of MS and is shown to induce intracellular glycolytic metabolism in pro-inflammatory microglia and macrophages, as well as CNS-resident astrocyt...

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Published in:International journal of molecular sciences 2017-02, Vol.18 (2), p.421-421
Main Authors: Wetzels, Suzan, Wouters, Kristiaan, Schalkwijk, Casper G, Vanmierlo, Tim, Hendriks, Jerome J A
Format: Article
Language:English
Subjects:
Adaptive Immunity
advanced glycation endproducts
Animals
Glycation End Products, Advanced - metabolism
Glycolysis
glyoxalase system
Humans
Immunity, Innate
Lipid Peroxidation
methylglyoxal
Multiple sclerosis
Multiple Sclerosis - immunology
Multiple Sclerosis - metabolism
Oxidation-Reduction
Oxidative Stress
Pyruvaldehyde - metabolism
Receptor for Advanced Glycation End Products - metabolism
receptor for advanced glycation endproduct
Review
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Summary:Multiple sclerosis (MS) is a demyelinating disease of the central nervous system (CNS). The activation of inflammatory cells is crucial for the development of MS and is shown to induce intracellular glycolytic metabolism in pro-inflammatory microglia and macrophages, as well as CNS-resident astrocytes. Advanced glycation endproducts (AGEs) are stable endproducts formed by a reaction of the dicarbonyl compounds methylglyoxal (MGO) and glyoxal (GO) with amino acids in proteins, during glycolysis. This suggests that, in MS, MGO-derived AGEs are formed in glycolysis-driven cells. MGO and MGO-derived AGEs can further activate inflammatory cells by binding to the receptor for advanced glycation endproducts (RAGE). Recent studies have revealed that AGEs are increased in the plasma and brain of MS patients. Therefore, AGEs might contribute to the inflammatory status in MS. Moreover, the main detoxification system of dicarbonyl compounds, the glyoxalase system, seems to be affected in MS patients, which may contribute to high MGO-derived AGE levels. Altogether, evidence is emerging for a contributing role of AGEs in the pathology of MS. In this review, we provide an overview of the current knowledge on the involvement of AGEs in MS.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms18020421