Suppr超能文献

衰老与糖尿病中胶原蛋白的非酶糖基化作用

Nonenzymatic glycation of collagen in aging and diabetes.

作者信息

Reiser K M

机构信息

Department of Medicine, School of Medicine, University of California, Davis 95616.

出版信息

Proc Soc Exp Biol Med. 1991 Jan;196(1):17-29. doi: 10.3181/00379727-196-43158c.

Abstract

Considerable progress has been made in our understanding of nonenzymatic glycation of collagen, and the relationship between glycation of collagen and changes in connective tissue associated with aging and diabetes. Recent studies surveyed in this review suggest the following conclusions: 1. Collagen content of early glycation products does not appear to increase throughout the life span in normal human subjects, although small increases may occur that are linked to glycemic changes. These products are increased, relative to age-matched controls, in experimental diabetes and in diabetes mellitus in collagen from virtually all tissues analyzed. 2. Collagen content of browning products increases with aging and appears to be higher in diabetic subjects than in age-matched controls. Rates of accumulation may be accelerated in subpopulations of diabetic subjects at high risk for developing complications. 3. Increases in early glycation products do not appear to be associated with alterations in collagen solubility, thermal rupture time, or mechanical strength, nor is there an association with most diabetic complications. Alterations in these products may, however, affect conformation, ligand binding, lysyl oxidase-mediated cross-linking, and interactions between collagen and other macromolecules in the extracellular matrix. 4. Increased content of browning products is associated with many physicochemical changes in collagen as well as with long-term complications in diabetes mellitus. 5. Regulatory mechanisms have been identified in vivo that may serve to control or limit the formation of glycation products. 7. Pharmacologic agents have been identified that may be able to reduce collagen content of late glycation products. Despite the progress that has been made in this field, many areas of uncertainty and controversy exist. For example, there is not yet a consensus that the browning products associated with collagen exclusively comprise advanced Maillard products derived from nonenzymatically glycated residues. There is evidence that oxidative reactions involving lipids also play a role in generating fluorophores and chromophores that may alter properties of collagen. Thus, in the extracellular matrix collagen may be continuously modified by at least three very different processes: Maillard reactions, interactions with oxidizing lipids, and enzymatically mediated cross-linking. The interrelationships between these and possibly other posttranslational modifications remain a poorly understood area of great complexity.

摘要

在我们对胶原蛋白非酶糖基化的理解以及胶原蛋白糖基化与衰老和糖尿病相关的结缔组织变化之间的关系方面已经取得了相当大的进展。本综述中调查的近期研究表明了以下结论:1. 在正常人类受试者中,早期糖基化产物的胶原蛋白含量在整个生命周期中似乎没有增加,尽管可能会出现与血糖变化相关的小幅增加。相对于年龄匹配的对照组,在实验性糖尿病以及几乎所有分析组织的糖尿病患者的胶原蛋白中,这些产物有所增加。2. 褐变产物的胶原蛋白含量随衰老而增加,并且在糖尿病患者中似乎高于年龄匹配的对照组。在有发生并发症高风险的糖尿病患者亚组中,积累速率可能会加快。3. 早期糖基化产物的增加似乎与胶原蛋白的溶解度、热破裂时间或机械强度的改变无关,也与大多数糖尿病并发症无关。然而,这些产物的改变可能会影响构象、配体结合、赖氨酰氧化酶介导的交联以及胶原蛋白与细胞外基质中其他大分子之间的相互作用。4. 褐变产物含量的增加与胶原蛋白的许多物理化学变化以及糖尿病的长期并发症有关。5. 已经在体内确定了可能用于控制或限制糖基化产物形成的调节机制。7. 已经确定了可能能够降低晚期糖基化产物胶原蛋白含量的药物制剂。尽管该领域已经取得了进展,但仍存在许多不确定和有争议的领域。例如,尚未达成共识,即与胶原蛋白相关的褐变产物仅包含源自非酶糖基化残基的晚期美拉德产物。有证据表明,涉及脂质的氧化反应在产生可能改变胶原蛋白特性的荧光团和发色团方面也起作用。因此,在细胞外基质中,胶原蛋白可能会通过至少三种非常不同的过程持续修饰:美拉德反应、与氧化脂质的相互作用以及酶介导的交联。这些以及可能其他翻译后修饰之间的相互关系仍然是一个非常复杂且了解甚少的领域。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验