Abstract：
Metabolism of fibronectin, the protein that plays a key role in the healing of wounds, is changed in the patients with diabetes mellitus. Fibronectin can interact with other proteins and proteoglycans and organise them to form the extracellular matrix, the basis of the granulation tissue in healing wounds. However, diabetic foot ulcers (DFUs) suffer from inadequate deposition of this protein. Degradation prevails over fibronectin synthesis in the proteolytic inflammatory environment in the ulcers. Because of the lack of fibronectin in the wound bed, the assembly of the extracellular matrix and the deposition of the granulation tissue cannot be started. A number of methods have been designed that prevents fibronectin degradation, replace lacking fibronectin or support its formation in non-healing wounds in animal models of diabetes. The aim of this article is to review the metabolism of fibronectin in DFUs and to emphasise that it would be useful to pay more attention to fibronectin matrix assembly in the ulcers when laboratory methods are translated to clinical practice.
摘要：
纤连蛋白的代谢，在伤口愈合中起关键作用的蛋白质，在糖尿病患者中发生了变化。纤连蛋白可以与其他蛋白质和蛋白聚糖相互作用，并组织它们形成细胞外基质，伤口愈合过程中肉芽组织的基础。然而,糖尿病足溃疡（DFU）患有这种蛋白质的沉积不足。在溃疡的蛋白水解炎症环境中，降解优于纤连蛋白的合成。因为伤口中缺乏纤连蛋白，细胞外基质的组装和肉芽组织的沉积不能开始。已经设计了许多防止纤连蛋白降解的方法，在糖尿病动物模型中替代缺乏纤连蛋白或支持其在不愈合伤口中的形成。本文的目的是回顾DFU中纤连蛋白的代谢，并强调将实验室方法转化为临床实践时，应更加关注溃疡中纤连蛋白基质的组装。
