Vashishth Deepak, Dhaliwal Ruban, Rubin Mishaela
Shirley Ann Jackson PhD. Center for Biotechnology and Interdisciplinary Studies, Rensselaer Polytechnic Institute, Troy, NY, United States of America; Department of Biomedical Engineering, Rensselaer Polytechnic Institute, Troy, NY, United States of America; Rensselaer - Icahn School of Medicine at Mount Sinai Center for Engineering and Precision Medicine, New York, NY, United States of America.
Division of Endocrinology, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX, United States of America.
Bone. 2025 Jan;190:117301. doi: 10.1016/j.bone.2024.117301. Epub 2024 Oct 21.
Advanced Glycation End-products (AGEs) are seen in long-lived proteins and were not expected to accumulate in the bone that turnovers and renews itself. Here, we provide a commentary on the contrary, highlighting the Special Issue of AGEs in Bone. An outcome of hyperglycemia and increased oxidative stress, AGEs form and accumulate by altering the bone resorption and formation processes. Accumulation of various AGEs species in bone increases bone fragility through the stiffening of the collagen network and, potentially, through the changes in collagen-mineral interactions. Evidence from both preclinical and clinical studies is leading to new translational approaches wherein measurement, inhibition, or removal of AGEs show the potential to diagnose, manage, and treat bone fragility associated with multiple conditions and diseases.
晚期糖基化终产物（AGEs）存在于长寿蛋白中，预计不会在不断更新换代的骨骼中积累。在此，我们提出相反的观点，重点介绍《骨骼中的AGEs》特刊。作为高血糖和氧化应激增加的结果，AGEs通过改变骨吸收和形成过程而形成并积累。骨骼中各种AGEs的积累会通过胶原蛋白网络的硬化以及可能通过胶原蛋白与矿物质相互作用的改变而增加骨骼脆性。临床前和临床研究的证据正在催生新的转化方法，其中AGEs的测量、抑制或清除显示出诊断、管理和治疗与多种病症和疾病相关的骨骼脆性的潜力。
