Advanced Glycation End Products Play Adverse Proinflammatory Activities in Osteoporosis

Osteoporosis is a major public health burden that is expected to further increase as the global population ages. In the last twenty years, advanced glycation end products (AGEs) have been shown to be critical mediators both in the pathogenesis and development of osteoporosis and other chronic degene...

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Main Authors: Roberta Sanguineti, Alessandra Puddu, François Mach, Fabrizio Montecucco, Giorgio Luciano Viviani
Format: Article
Language:English
Published: Wiley 2014-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2014/975872
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author Roberta Sanguineti
Alessandra Puddu
François Mach
Fabrizio Montecucco
Giorgio Luciano Viviani
author_facet Roberta Sanguineti
Alessandra Puddu
François Mach
Fabrizio Montecucco
Giorgio Luciano Viviani
author_sort Roberta Sanguineti
collection DOAJ
description Osteoporosis is a major public health burden that is expected to further increase as the global population ages. In the last twenty years, advanced glycation end products (AGEs) have been shown to be critical mediators both in the pathogenesis and development of osteoporosis and other chronic degenerative diseases related to aging. The accumulation of AGEs within the bone induces the formation of covalent cross-links with collagen and other bone proteins which affects the mechanical properties of tissue and disturbs bone remodelling and deterioration, underlying osteoporosis. On the other hand, the gradual deterioration of the immune system during aging (defined as immunosenescence) is also characterized by the generation of a high level of oxidants and AGEs. The synthesis and accumulation of AGEs (both localized within the bone or in the systemic circulation) might trigger a vicious circle (in which inflammation and aging merged in the word “Inflammaging”) which can establish and sustain the development of osteoporosis. This narrative review will update the molecular mechanisms/pathways by which AGEs induce the functional and structural bone impairment typical of osteoporosis.
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institution Kabale University
issn 0962-9351
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publishDate 2014-01-01
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series Mediators of Inflammation
spelling doaj-art-18b5ff2636874b30bd7496a39332e8512025-02-03T06:08:09ZengWileyMediators of Inflammation0962-93511466-18612014-01-01201410.1155/2014/975872975872Advanced Glycation End Products Play Adverse Proinflammatory Activities in OsteoporosisRoberta Sanguineti0Alessandra Puddu1François Mach2Fabrizio Montecucco3Giorgio Luciano Viviani4Department of Internal Medicine, University of Genoa, 6 Viale Benedetto XV, 16132 Genoa, ItalyDepartment of Internal Medicine, University of Genoa, 6 Viale Benedetto XV, 16132 Genoa, ItalyDivision of Cardiology, Foundation for Medical Researches, Faculty of Medicine, Geneva University Hospitals, 64 Avenue de la Roseraie, 1211 Geneva, SwitzerlandDivision of Cardiology, Foundation for Medical Researches, Faculty of Medicine, Geneva University Hospitals, 64 Avenue de la Roseraie, 1211 Geneva, SwitzerlandDepartment of Internal Medicine, University of Genoa, 6 Viale Benedetto XV, 16132 Genoa, ItalyOsteoporosis is a major public health burden that is expected to further increase as the global population ages. In the last twenty years, advanced glycation end products (AGEs) have been shown to be critical mediators both in the pathogenesis and development of osteoporosis and other chronic degenerative diseases related to aging. The accumulation of AGEs within the bone induces the formation of covalent cross-links with collagen and other bone proteins which affects the mechanical properties of tissue and disturbs bone remodelling and deterioration, underlying osteoporosis. On the other hand, the gradual deterioration of the immune system during aging (defined as immunosenescence) is also characterized by the generation of a high level of oxidants and AGEs. The synthesis and accumulation of AGEs (both localized within the bone or in the systemic circulation) might trigger a vicious circle (in which inflammation and aging merged in the word “Inflammaging”) which can establish and sustain the development of osteoporosis. This narrative review will update the molecular mechanisms/pathways by which AGEs induce the functional and structural bone impairment typical of osteoporosis.http://dx.doi.org/10.1155/2014/975872
spellingShingle Roberta Sanguineti
Alessandra Puddu
François Mach
Fabrizio Montecucco
Giorgio Luciano Viviani
Advanced Glycation End Products Play Adverse Proinflammatory Activities in Osteoporosis
Mediators of Inflammation
title Advanced Glycation End Products Play Adverse Proinflammatory Activities in Osteoporosis
title_full Advanced Glycation End Products Play Adverse Proinflammatory Activities in Osteoporosis
title_fullStr Advanced Glycation End Products Play Adverse Proinflammatory Activities in Osteoporosis
title_full_unstemmed Advanced Glycation End Products Play Adverse Proinflammatory Activities in Osteoporosis
title_short Advanced Glycation End Products Play Adverse Proinflammatory Activities in Osteoporosis
title_sort advanced glycation end products play adverse proinflammatory activities in osteoporosis
url http://dx.doi.org/10.1155/2014/975872
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