Ott Christiane, Jacobs Kathleen, Haucke Elisa, Navarrete Santos Anne, Grune Tilman, Simm Andreas
Department of Nutritional Toxicology, Institute of Nutrition, Friedrich Schiller University Jena, 07743 Jena, Germany.
Clinic for Cardiothoracic Surgery, University Hospital Halle (Saale), Martin-Luther-University of Halle-Wittenberg, Ernst-Grube Strasse 40, D-06120 Halle (Saale), Germany.
Redox Biol. 2014 Jan 9;2:411-29. doi: 10.1016/j.redox.2013.12.016. eCollection 2014.
Improvements in health care and lifestyle have led to an elevated lifespan and increased focus on age-associated diseases, such as neurodegeneration, cardiovascular disease, frailty and arteriosclerosis. In all these chronic diseases protein, lipid or nucleic acid modifications are involved, including cross-linked and non-degradable aggregates, such as advanced glycation end products (AGEs). Formation of endogenous or uptake of dietary AGEs can lead to further protein modifications and activation of several inflammatory signaling pathways. This review will give an overview of the most prominent AGE-mediated signaling cascades, AGE receptor interactions, prevention of AGE formation and the impact of AGEs during pathophysiological processes.
医疗保健和生活方式的改善使寿命延长,人们越来越关注与年龄相关的疾病,如神经退行性变、心血管疾病、身体虚弱和动脉硬化。在所有这些慢性疾病中,都涉及蛋白质、脂质或核酸修饰,包括交联和不可降解的聚集体,如晚期糖基化终产物(AGEs)。内源性AGEs的形成或膳食AGEs的摄入会导致进一步的蛋白质修饰,并激活多种炎症信号通路。本综述将概述最突出的AGE介导的信号级联反应、AGE受体相互作用、AGE形成的预防以及AGEs在病理生理过程中的影响。