非酶糖基化对糖尿病和年龄相关骨脆性中胶原纳米级机制的影响。

Pub Date : 2023-06-21 DOI:10.32604/biocell.2023.028014
James L Rosenberg, William Woolley, Ihsan Elnunu, Julia Kamml, David S Kammer, Claire Acevedo
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引用次数: 0

摘要

人们早就知道,年龄和糖尿病会诱导葡萄糖和胶原蛋白之间的氧化反应,导致胶原组织中晚期糖基化终产物(AGEs)交联的积累。最近,AGEs的含量与骨质量的丧失有关,与骨量无关,与衰老和糖尿病患者骨折风险增加有关。骨质量的丧失主要归因于材料性质、结构组织或细胞重塑的变化。虽然所有这些因素都在骨质疏松症中发挥作用,但在糖尿病和年龄相关的骨质疏松症之间可以发现一些共同的反复出现的模式。我们将在这一观点中讨论的主要模式是随着AGE的积累,原纤维胶原硬度的增加和胶原诱导的可塑性的丧失。本研究结合近年来的相关实验研究,探讨了荧光AGEs在分子和纤维尺度上的含量,在纳米尺度上的胶原变形机制,以及在宏观尺度上的抗骨折性之间的相关性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Effect of non-enzymatic glycation on collagen nanoscale mechanisms in diabetic and age-related bone fragility.

Effect of non-enzymatic glycation on collagen nanoscale mechanisms in diabetic and age-related bone fragility.

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Effect of non-enzymatic glycation on collagen nanoscale mechanisms in diabetic and age-related bone fragility.

Age and diabetes have long been known to induce an oxidative reaction between glucose and collagen, leading to the accumulation of advanced glycation end-products (AGEs) cross-links in collagenous tissues. More recently, AGEs content has been related to loss of bone quality, independent of bone mass, and increased fracture risk with aging and diabetes. Loss of bone quality is mostly attributed to changes in material properties, structural organization, or cellular remodeling. Though all these factors play a role in bone fragility disease, some common recurring patterns can be found between diabetic and age-related bone fragility. The main pattern we will discuss in this viewpoint is the increase of fibrillar collagen stiffness and loss of collagen-induced plasticity with AGE accumulation. This study focused on recent related experimental studies and discusses the correlation between fluorescent AGEs content at the molecular and fibrillar scales, collagen deformation mechanisms at the nanoscale, and resistance to bone fracture at the macroscale.

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