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Aging and disease    2018, Vol. 9 Issue (5) : 880-900     DOI: 10.14336/AD.2017.1121
Review |
Glycation Damage: A Possible Hub for Major Pathophysiological Disorders and Aging
Maxime Fournet1, Frédéric Bonté2, Alexis Desmoulière3,*
1University of Limoges, Faculty of Pharmacy, Department of Physiology, EA 6309, F-87025 Limoges, France
2LVMH Recherche, F-45800 St-Jean-de-Braye, France
3University of Limoges, Faculty of Pharmacy, Department of Physiology, EA 6309, F-87025 Limoges, France
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Abstract  

Glycation is both a physiological and pathological process which mainly affects proteins, nucleic acids and lipids. Exogenous and endogenous glycation produces deleterious reactions that take place principally in the extracellular matrix environment or within the cell cytosol and organelles. Advanced glycation end product (AGE) formation begins by the non-enzymatic glycation of free amino groups by sugars and aldehydes which leads to a succession of rearrangements of intermediate compounds and ultimately to irreversibly bound products known as AGEs. Epigenetic factors, oxidative stress, UV and nutrition are important causes of the accumulation of chemically and structurally different AGEs with various biological reactivities. Cross-linked proteins, deriving from the glycation process, present both an altered structure and function. Nucleotides and lipids are particularly vulnerable targets which can in turn favor DNA mutation or a decrease in cell membrane integrity and associated biological pathways respectively. In mitochondria, the consequences of glycation can alter bioenergy production. Under physiological conditions, anti-glycation defenses are sufficient, with proteasomes preventing accumulation of glycated proteins, while lipid turnover clears glycated products and nucleotide excision repair removes glycated nucleotides. If this does not occur, glycation damage accumulates, and pathologies may develop. Glycation-induced biological products are known to be mainly associated with aging, neurodegenerative disorders, diabetes and its complications, atherosclerosis, renal failure, immunological changes, retinopathy, skin photoaging, osteoporosis, and progression of some tumors.

Keywords exogenous glycation      endogenous glycation      advanced glycation end product      aging      neurodegenerative disorders      diabetes     
Corresponding Authors: Alexis Desmouliere   
About author: These authors contributed equally to this work.
Issue Date: 22 September 2017
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Fournet Maxime
Bonté Frédéric
Desmoulière Alexis
Cite this article:   
Fournet Maxime,Bonté Frédéric,Desmoulière Alexis. Glycation Damage: A Possible Hub for Major Pathophysiological Disorders and Aging[J]. Aging and disease, 2018, 9(5): 880-900.
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http://www.aginganddisease.org/EN/10.14336/AD.2017.1121     OR     http://www.aginganddisease.org/EN/Y2018/V9/I5/880
Figure 1.  In vivo glycation processes.
Figure 2.  All AGEs formed in the body due to glycation and four other metabolic pathways.
Glycation within the dermal and epidermal extracellular matrix
➢ Increased rigidity of the skin and decreased elasticity
➢ Activation of RAGE: secretion of cytokines and growth factors
➢ Induction of senescence and apoptosis in fibroblasts and disruption of keratinocytes
➢ Changes in the synthesis of components of the extracellular matrix and of metalloproteinases
Intracellular glycation
➢ Decreased effectiveness of the proteasome when its enzymes are affected by glycation
➢ Accumulation of glycated vimentin within fibroblasts and decreased contractile activity of these cells in collagen gels
Effects of UV rays
➢ Effect of UVA rays on certain AGEs in the skin: stimulation of the products of reactive oxygen species, which are not eliminated as effectively following the glycation of catalase and superoxide dismutase
➢ Stimulation of the production of AGEs and of the expression of RAGEs in the skin due to exposure to sunlight
Table 1  Summary of effects (suggested by various studies) of glycation on skin aging.
Figure 3.  Diagram of the effects (suggested by various studies) of glycation on skin aging.
Figure 4.  Carboxymethyl-lysine immunostaining (red) on normal human skin: glycated (A) and non-glycated (B) areas

Nuclei are stained using DAPI (blue). E: epidermis; D: dermis. Magnification x200.

Figure 5.  The role played by stimulated RAGEs in Alzheimer’s disease as suggested by various studies.
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