Bierhaus A, Ziegler R, Nawroth P P
Medizinische Klinik I der Universität Heidelberg, Deutschland.
Horm Res. 1998;50 Suppl 1:1-5. doi: 10.1159/000053094.
Advanced glycation end products (AGEs), known to accumulate during aging and at accelerated rate during the course of diabetes, have been demonstrated to induce changes in endothelial properties that might contribute to the pathogenesis of micro- and macroangiopathy. Since AGE-formation not only changes the physicochemical properties of proteins, but also induces cellular signalling, activation of transcription factors and subsequent gene expression, AGEs are now regarded as important mediators of diabetic vascular disease. The growing knowledge on the molecular mechanisms underlying the AGE-dependent activation of vascular endothelial cells implicates possible new therapeutic interventions in the therapy of diabetic angiopathy.
晚期糖基化终末产物(AGEs)在衰老过程中会逐渐积累,而在糖尿病病程中其积累速度会加快。研究表明,AGEs会引起内皮细胞特性的改变,这可能与微血管和大血管病变的发病机制有关。由于AGE的形成不仅会改变蛋白质的物理化学性质,还会诱导细胞信号传导、激活转录因子并随后影响基因表达,因此AGEs现在被认为是糖尿病血管疾病的重要介质。对AGE依赖的血管内皮细胞激活的分子机制的深入了解,为糖尿病血管病变的治疗提供了可能的新治疗干预措施。