Advanced glycation end-product (AGE) is the generic term for a heterogeneous group of derivatives arising from a non-enzymatic reaction between reducing sugars and proteins. In recent years, evidence has accumulated that incriminates AGEs in pathogenic processes associated with both chronic hyperglycaemia and age-related diseases. Regardless of their exogenous or endogenous origin, the accumulation of AGEs and their derivatives could promote accelerated ageing by leading to protein modifications and activating several inflammatory signalling pathways via AGE-specific receptors. However, it remains to be demonstrated whether preventing the accumulation of AGEs and their effects is an important therapeutic option for successful ageing. The present review gives an overview of the current knowledge on the pathogenic role of AGEs by focusing on three AGE target organs: kidney, heart and brain. For each of these organs we concentrate on an age-related disease, each of which is a major public health issue: chronic kidney disease, heart dysfunction and neurodegenerative diseases. Even though strong connections have been highlighted between glycation and age-related pathogenesis, causal links still need to be validated. In each case, we report evidence and uncertainties suggested by animal or epidemiological studies on the possible link between pathogenesis and glycation in a chronic hyperglycaemic state, in the absence of diabetes, and with exogenous AGEs alone. Finally, we present some promising anti-AGE strategies that are currently being studied.
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June 2017
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The accompanying caption is: Image demonstrates a 3D reconstruction of the neurovascular unit in a hippocampal artery in the mouse brain. For further details, see article by Nizari et al in this issue, pages 1207-1214. Image kindly provided by Cheryl Hawkes.
Review Article|
May 17 2017
Kidney, heart and brain: three organs targeted by ageing and glycation
Marie Frimat;
1University of Lille, INSERM, CHU Lille, U995–LIRIC–Lille Inflammation Research International Centre, F-59000 Lille, France
2Nephrology Department, CHU Lille, F-59000 Lille, France
Correspondence: Marie Frimat ([email protected]) or Eric Boulanger ([email protected])
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Maité Daroux;
Maité Daroux
1University of Lille, INSERM, CHU Lille, U995–LIRIC–Lille Inflammation Research International Centre, F-59000 Lille, France
3Nephrology Department, Duchenne Hospital, Boulogne sur Mer, France
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Rachel Litke;
Rachel Litke
1University of Lille, INSERM, CHU Lille, U995–LIRIC–Lille Inflammation Research International Centre, F-59000 Lille, France
4Geriatric Department, CHU Lille, F-59000 Lille, France
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Rémi Nevière;
Rémi Nevière
1University of Lille, INSERM, CHU Lille, U995–LIRIC–Lille Inflammation Research International Centre, F-59000 Lille, France
5Physiology Department, CHU Lille, F-59000 Lille, France
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Frédéric J. Tessier;
Frédéric J. Tessier
1University of Lille, INSERM, CHU Lille, U995–LIRIC–Lille Inflammation Research International Centre, F-59000 Lille, France
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Eric Boulanger
1University of Lille, INSERM, CHU Lille, U995–LIRIC–Lille Inflammation Research International Centre, F-59000 Lille, France
4Geriatric Department, CHU Lille, F-59000 Lille, France
Correspondence: Marie Frimat ([email protected]) or Eric Boulanger ([email protected])
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Publisher: Portland Press Ltd
Received:
October 28 2016
Revision Received:
February 01 2017
Accepted:
February 06 2017
Online ISSN: 1470-8736
Print ISSN: 0143-5221
© 2017 The Author(s). published by Portland Press Limited on behalf of the Biochemical Society
2017
Clin Sci (Lond) (2017) 131 (11): 1069–1092.
Article history
Received:
October 28 2016
Revision Received:
February 01 2017
Accepted:
February 06 2017
Citation
Marie Frimat, Maité Daroux, Rachel Litke, Rémi Nevière, Frédéric J. Tessier, Eric Boulanger; Kidney, heart and brain: three organs targeted by ageing and glycation. Clin Sci (Lond) 1 June 2017; 131 (11): 1069–1092. doi: https://doi.org/10.1042/CS20160823
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