Role of advanced glycated end products in mediating diabetes associated atherosclerosis

糖尿病在西方世界正在增加，随着这种增加，并发症的负担也在增加。其中之一是动脉粥样硬化，它会导致心脏病发作、中风和坏疽。在这项资助中，我们考虑了糖与蛋白质结合的生化反应的作用，这种反应被称为晚期糖化，以及它如何促进动脉粥样硬化。我们将使用新的药物来阻断易患动脉粥样硬化的糖尿病小鼠模型的血管损伤。我们还将这些糖连接蛋白（AGEs）注射到小鼠体内，以观察它们如何直接影响血管壁。我们将描述响应这些AGEs的分子和细胞变化。这些研究将最终导致更好的治疗方法，以预防，减缓或逆转糖尿病的血管损伤。

Diabetes is on the increase in the Western world and with this increase comes the burden of increased complications. One of these is atherosclerosis which leads to heart attacks, strokes and gangrene. In this grant we consider the role of a biochemical reaction where sugar attaches to proteins called advanced glycation and how it may promote atherosclerosis. We will use novel drugs to block vessel damage in a model of diabetic mice prone to atherosclerosis. We will also inject these sugar-attached proteins (AGEs) into mice to see how they directly influence the vessel wall. We will characterise molecular and cellular changes in response to these AGEs. These studies will ultimately lead to better treatments to prevent, slow down or reverse blood vessel damage in diabetes.