摘要
背景:糖尿病(DM)是一种常见的代谢紊乱,其特征是血糖持续升高。2型糖尿病的特点是胰岛素抵抗和β细胞功能障碍。硫氧还蛋白相互作用蛋白(TXNIP)是控制胰腺β-细胞产生和丢失的因素之一。 目的:近期研究表明,高糖可显著上调TXNIP的表达。TXNIP在β细胞中过表达不仅能诱导细胞凋亡,还能减少胰岛素的分泌。同时,TXNIP缺乏保护β细胞凋亡,导致胰岛素分泌增加。因此,寻找可以调节TXNIP表达和下游信号通路的小分子是至关重要的。因此,抑制TXNIP对糖尿病患者心血管系统及心脏、肾脏等组织均有有益作用。因此,糖尿病治疗必须针对TXNIP的小分子活性,抑制表达,促进内源性细胞数量和胰岛素的产生。 结论:本文综述了TXNIP的作用机制、调控机制及晶体结构。此外,我们强调了TXNIP信号网络如何促进糖尿病,并与抑制糖尿病发展的药物相互作用及其复合物。最后,对TXNIP靶向治疗的现状和前景进行了展望。
关键词: TXNIP、β细胞、DM、FOXO1、ChREBP、胰岛素。
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