Department of Anesthesiology, The Second Affiliated Hospital of Nanchang University, Nanchang, China.
Department of Clinical Medicine, The Second Clinical Medical College of Nanchang University, Nanchang, China.
Diabetes Metab Res Rev. 2024 Sep;40(6):e3841. doi: 10.1002/dmrr.3841.
Diabetic encephalopathy (DE) is a severe complication that occurs in the central nervous system (CNS) and leads to cognitive impairment. DE involves various pathophysiological processes, and its pathogenesis is still unclear. This review summarised current research on the pathogenesis of diabetic encephalopathy, which involves neuroinflammation, oxidative stress, iron homoeostasis, blood-brain barrier disruption, altered gut microbiota, insulin resistance, etc. Among these pathological mechanisms, neuroinflammation has been focused on. This paper summarises some of the molecular mechanisms involved in neuroinflammation, including the Mammalian Target of Rapamycin (mTOR), Lipocalin-2 (LCN-2), Pyroptosis, Advanced Glycosylation End Products (AGEs), and some common pro-inflammatory factors. In addition, we discuss recent advances in the study of potential therapeutic targets for the treatment of DE against neuroinflammation. The current research on the pathogenesis of DE is progressing slowly, and more research is needed in the future. Further study of neuroinflammation as a mechanism is conducive to the discovery of more effective treatments for DE in the future.
糖尿病性脑病（DE）是一种发生在中枢神经系统（CNS）的严重并发症，可导致认知障碍。DE 涉及多种病理生理过程，其发病机制尚不清楚。本综述总结了目前关于糖尿病性脑病发病机制的研究，涉及神经炎症、氧化应激、铁稳态、血脑屏障破坏、肠道微生物群改变、胰岛素抵抗等。在这些病理机制中，神经炎症受到了关注。本文总结了神经炎症涉及的一些分子机制，包括雷帕霉素靶蛋白（mTOR）、载脂蛋白 L（LCN-2）、细胞焦亡、晚期糖基化终产物（AGEs）和一些常见的促炎因子。此外，我们还讨论了针对神经炎症治疗 DE 的潜在治疗靶点研究的最新进展。目前 DE 发病机制的研究进展缓慢，未来还需要更多的研究。进一步研究神经炎症作为一种机制，有助于未来发现更有效的 DE 治疗方法。
