Shen Chieh-Yu, Lu Cheng-Hsun, Cheng Chiao-Feng, Li Ko-Jen, Kuo Yu-Min, Wu Cheng-Han, Liu Chin-Hsiu, Hsieh Song-Chou, Tsai Chang-Youh, Yu Chia-Li
Department of Internal Medicine, National Taiwan University Hospital, National Taiwan University College of Medicine, # 7 Chung-Shan South Road, Taipei 10002, Taiwan.
Institute of Clinical Medicine, National Taiwan University College of Medicine, # 7 Chung-Shan South Road, Taipei 10002, Taiwan.
Biomedicines. 2024 Jul 31;12(8):1699. doi: 10.3390/biomedicines12081699.
Increased production of advanced glycation end products (AGEs) among reducing sugars (glucose, fructose, galactose, or ribose) and amino acids/proteins via non-enzymatic Maillard reaction can be found in lifestyle-related disease (LSRD), metabolic syndrome (MetS), and obesity and immune-related diseases. Increased serum levels of AGEs may induce aging, diabetic complications, cardiovascular diseases (CVD), neurodegenerative diseases (NDD), cancer, and inflamm-aging (inflammation with immunosenescence). The Maillard reaction can also occur among reducing sugars and lipoproteins or DNAs to alter their structure and induce immunogenicity/genotoxicity for carcinogenesis. AGEs, as danger-associated molecular pattern molecules (DAMPs), operate via binding to receptor for AGE (RAGE) or other scavenger receptors on cell surface to activate PI3K-Akt-, P38-MAPK-, ERK1/2-JNK-, and MyD88-induced NF-κB signaling pathways to mediate various pathological effects. Recently, the concept of "inflamm-aging" became more defined, and we have unveiled some interesting findings in relation to it. The purpose of the present review is to dissect the potential molecular basis of inflamm-aging in patients with diabetes and immune-mediated diseases caused by different AGEs.
在生活方式相关疾病(LSRD)、代谢综合征(MetS)、肥胖症以及免疫相关疾病中,均可发现还原糖(葡萄糖、果糖、半乳糖或核糖)与氨基酸/蛋白质通过非酶促美拉德反应生成晚期糖基化终末产物(AGEs)的量增加。血清中AGEs水平升高可能会引发衰老、糖尿病并发症、心血管疾病(CVD)、神经退行性疾病(NDD)、癌症以及炎症衰老(伴有免疫衰老的炎症)。美拉德反应也可能发生在还原糖与脂蛋白或DNA之间,从而改变它们的结构并诱导免疫原性/基因毒性,进而引发癌症。作为危险相关分子模式分子(DAMPs),AGEs通过与细胞表面的AGE受体(RAGE)或其他清道夫受体结合,激活PI3K-Akt-、P38-MAPK-、ERK1/2-JNK-以及MyD88诱导的NF-κB信号通路,以介导各种病理效应。最近,“炎症衰老”的概念变得更加明确,并且我们已经揭示了一些与之相关的有趣发现。本综述的目的是剖析糖尿病患者以及由不同AGEs引起的免疫介导疾病中炎症衰老的潜在分子基础。