II Faculty and Clinic of Obstetrics and Gynaecology, Medical University of Warsaw, 00-315 Warsaw, Poland.
Doctoral School, Medical University of Warsaw, Zwirki i Wigury 81, 02-091 Warsaw, Poland.
Int J Mol Sci. 2023 Jul 1;24(13):10982. doi: 10.3390/ijms241310982.
Advanced glycation end products (AGEs) are mediators in the process of cellular dysfunction in response to hyperglycemia. Numerous data indicate that the accumulation of AGEs in the extracellular matrix plays a key role in the development of obesity-related adipose tissue dysfunction. Through binding of their membrane receptor (), AGEs affect numerous intracellular pathways and impair adipocyte differentiation, metabolism, and secretory activity. Therefore, inhibiting the production and accumulation of AGEs, as well as interfering with the metabolic pathways they activate, may be a promising therapeutic strategy for restoring normal adipose tissue function and, thus, combating obesity-related comorbidities. This narrative review summarizes data on the involvement of the pathway in adipose tissue dysfunction in obesity and the development of its metabolic complications. The paper begins with a brief review of AGE synthesis and the signaling pathway. The effect of the pathway on adipose tissue development and activity is then presented. Next, data from animal and human studies on the involvement of the pathway in obesity, diabetes, and cardiovascular diseases are summarized. Finally, therapeutic perspectives based on interference with the pathway are discussed.
糖基化终产物 (AGEs) 是细胞功能障碍反应高血糖的中介物。大量数据表明，细胞外基质中 AGEs 的积累在肥胖相关脂肪组织功能障碍的发展中起着关键作用。通过其膜受体 () 的结合，AGEs 影响众多细胞内途径，并损害脂肪细胞分化、代谢和分泌活性。因此，抑制 AGEs 的产生和积累，以及干扰它们激活的代谢途径，可能是恢复正常脂肪组织功能并因此对抗肥胖相关合并症的有前途的治疗策略。本综述总结了关于 途径在肥胖症中脂肪组织功能障碍及其代谢并发症发展中的作用的数据。本文首先简要回顾了 AGE 的合成和 信号通路。然后介绍了 途径对脂肪组织发育和活性的影响。接下来，总结了关于 途径在肥胖症、糖尿病和心血管疾病中的作用的动物和人类研究数据。最后，讨论了基于干扰 途径的治疗前景。
