Department of Nephrology, Klinikum rechts der Isar, Technical University Munich, Ismaninger Str, 22, 81675 Munich, Germany.
Crit Care. 2009;13(4):164. doi: 10.1186/cc7939. Epub 2009 Jul 14.
Advanced glycation endproducts (AGEs) are primarily known as a complication in diabetic patients through their mediation of the inflammatory response. However, a variety of studies have demonstrated enhanced formation of AGEs in cardiovascular disorders. Despite the large number of AGEs produced during the Maillard reaction, recent focus is on the major non-crosslinking AGE Nepsilon-carboxymethyllysine. Kneyber and colleagues focused on sepsis-induced cardiac dysfunction and investigated whether myocardial inflammation is associated with enhanced cardiac AGE deposition and whether this is further enhanced by mechanical ventilation. They showed that both conditions are associated with enhanced AGE deposition and myocardial inflammation. Therefore, AGEs may participate in the inflammatory response related to cardiac dysfunction in critically ill patients. Moreover, life-saving ventilation stimulates AGE formation in these patients. This interesting study raises the question of whether AGEs in critically ill patients are a driving force of the disease.
糖基化终产物(AGEs)主要通过介导炎症反应,成为糖尿病患者的一种并发症。然而,许多研究已经证明,心血管疾病中 AGEs 的形成会增强。尽管在美拉德反应过程中会产生大量的 AGEs,但最近的研究重点是主要的非交联 AGE Nepsilon-羧甲基赖氨酸。Kneyber 及其同事专注于脓毒症引起的心脏功能障碍,并研究心肌炎症是否与增强的心脏 AGE 沉积有关,以及机械通气是否会进一步增强这种情况。他们表明,这两种情况都与增强的 AGE 沉积和心肌炎症有关。因此,AGEs 可能参与与危重病患者心脏功能障碍相关的炎症反应。此外,挽救生命的通气会刺激这些患者的 AGE 形成。这项有趣的研究提出了一个问题,即在危重病患者中,AGEs 是否是疾病的驱动力。