Sanguineti Roberta, Puddu Alessandra, Mach François, Montecucco Fabrizio, Viviani Giorgio Luciano
Department of Internal Medicine, University of Genoa, 6 Viale Benedetto XV, 16132 Genoa, Italy.
Division of Cardiology, Foundation for Medical Researches, Faculty of Medicine, Geneva University Hospitals, 64 Avenue de la Roseraie, 1211 Geneva, Switzerland.
Mediators Inflamm. 2014;2014:975872. doi: 10.1155/2014/975872. Epub 2014 Mar 20.
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.
骨质疏松症是一项重大的公共卫生负担，随着全球人口老龄化，预计这一负担还会进一步加重。在过去二十年中，晚期糖基化终末产物（AGEs）已被证明是骨质疏松症及其他与衰老相关的慢性退行性疾病发病机制和发展过程中的关键介质。AGEs在骨骼中的积累会诱导其与胶原蛋白及其他骨蛋白形成共价交联，从而影响组织的力学性能，扰乱骨重塑和骨退化，这是骨质疏松症的潜在病因。另一方面，衰老过程中免疫系统的逐渐衰退（即免疫衰老）也表现为高水平氧化剂和AGEs的产生。AGEs的合成与积累（无论是在骨骼局部还是在体循环中）可能会引发恶性循环（“炎症衰老”一词将炎症与衰老联系在一起），进而引发并维持骨质疏松症的发展。本叙述性综述将更新AGEs诱导骨质疏松症典型的功能性和结构性骨损伤的分子机制/途径。
