胰岛B细胞丢失是T1DM和T2DM发病的关键因素,但目前尚缺少治疗的办法。该文作者们最近发现,硫还原素-相互作用蛋白(TXNIP)是一种处处表达的细胞氧化还原调节因子,可作为这方面很有吸引力的新靶标。TXNIP增加糖尿病过度表达引起胰岛β细胞凋亡,是糖毒性引起胰岛p细胞死亡的首要原因。相反,TXNIP的遗传消融促进内生胰岛β细胞生存并预 Islet B cell loss is a key factor in the pathogenesis of T1DM and T2DM, but the treatment is still lacking. The authors recently found that the sulfur-reduced-interacting protein (TXNIP) is an overexpressing cellular redox regulator that serves as a promising new target in this regard. TXNIP increased diabetes over-expression caused by pancreatic β-cell apoptosis, is the first cause of glucose toxicity caused by islet p cell death. In contrast, genetic ablation of TXNIP promotes endogenous islet beta cell survival and preconditioning