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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DOI:
10.32604/biocell.2023.028014
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发表时间:
2023-06-21
期刊:
Biocell : official journal of the Sociedades Latinoamericanas de Microscopia Electronica ... et. al
影响因子:
--
通讯作者:
Acevedo C
Acevedo C
中科院分区:
其他
文献类型:
--
作者:
Rosenberg JL;Woolley W;Elnunu I;Kamml J;Kammer DS;Acevedo C

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糖基化终末产物(AGEs)和糖尿病长期以来一直被认为是诱导葡萄糖和胶原之间的氧化反应,导致晚期糖基化终末产物(AGEs)在胶原组织中积累的交联物。最近,AGEs的含量与骨骼质量的丧失有关,与骨量无关,并随着年龄和糖尿病的增加而增加骨折风险。骨质量的丧失主要归因于材料特性、结构组织或细胞重塑的改变。尽管所有这些因素都在骨脆性疾病中发挥了作用,但在糖尿病和年龄相关性骨脆性之间可以发现一些常见的复发模式。我们将在这一观点中讨论的主要模式是随着年龄的积累,胶原纤维硬度的增加和胶原诱导的可塑性的丧失。本研究重点介绍了近年来相关的实验研究,并讨论了分子和纤维尺度上的荧光AGEs含量、纳米尺度上的胶原变形机制和宏观尺度上的抗骨折力之间的相关性。
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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