The Buck Institute for Research on Aging, 8001 Redwood Boulevard, Novato, CA 94945, USA.
Touro University College of Osteopathic Medicine, Glycation Oxidation and Research laboratory, Vallejo, CA, 94592, USA.
Cell Metab. 2018 Sep 4;28(3):337-352. doi: 10.1016/j.cmet.2018.08.014.
Accumulation of advanced glycation end products (AGEs) on nucleotides, lipids, and peptides/proteins are an inevitable component of the aging process in all eukaryotic organisms, including humans. To date, a substantial body of evidence shows that AGEs and their functionally compromised adducts are linked to and perhaps responsible for changes seen during aging and for the development of many age-related morbidities. However, much remains to be learned about the biology of AGE formation, causal nature of these associations, and whether new interventions might be developed that will prevent or reduce the negative impact of AGEs-related damage. To facilitate achieving these latter ends, we show how invertebrate models, notably Drosophila melanogaster and Caenorhabditis elegans, can be used to explore AGE-related pathways in depth and to identify and assess drugs that will mitigate against the detrimental effects of AGE-adduct development.
在所有真核生物（包括人类）的衰老过程中，核苷酸、脂质和肽/蛋白质上的高级糖基化终产物（AGEs）的积累是不可避免的组成部分。迄今为止，大量证据表明，AGEs 及其功能受损的加合物与衰老过程中观察到的变化以及许多与年龄相关的疾病的发生有关，甚至可能是其原因。然而，关于 AGE 形成的生物学、这些关联的因果性质，以及是否可能开发出新的干预措施来预防或减少与 AGE 相关损伤的负面影响，仍有许多需要了解。为了促进实现这些目标，我们展示了如何使用无脊椎动物模型（尤其是黑腹果蝇和秀丽隐杆线虫）深入研究 AGE 相关途径，并识别和评估可减轻 AGE 加合物形成的有害影响的药物。
