摘要
硫氧还蛋白(TRX)相互作用蛋白(TXNIP)在氧化还原、细胞增殖、细胞凋亡、血脂和血糖代谢等过程中发挥多重作用。大量研究表明,高糖可以通过碳水化合物反应元件结合蛋白(ChREBP)、p38丝裂原活化蛋白激酶(p38MAPK)、叉头框转录因子O亚族1(FOX01)途径引起TXNIP表达增多,过多的TXNIP主要通过介导氧化应激和炎性反应两条途径引起胰岛β细胞损害、胰岛功能下降及胰岛素抵抗。且TXNIP在糖尿病视网膜病变、糖尿病肾病的发生、发展中也起重要作用。
Thioredoxin-interacting protein (TXNIP) plays an important role in regulation of oxida- tion-reduction process, cell proliferation, cell apoptosis and glucose-lipid matabolism. Studies indicated that high glucose can induce the overexpression of TXNIP through carbohydrate response element-binding protein (ChREBP), p38 mitogen-activated protein kinase (p38MAPK), forkhead box transcription factor O1 ( FOXO1 )pathways and overexpression of TXNIP can lead to impairment of βcells, dysfunction of pancreatic islet and insulin resistance through oxidative stress and inflammation. In addition, TXNIP also plays an impor- tant role in the occurrence and development of diabetic nephropathy, diabetic retinopathy.
出处
《国际内分泌代谢杂志》
北大核心
2013年第1期53-55,共3页
International Journal of Endocrinology and Metabolism