PDF(Pubmed)
Abstract：
The prevalence of diabetes is increasing worldwide. Massive death of pancreatic beta-cells causes type 1 diabetes. Progressive loss of beta-cell function and mass characterizes type 2 diabetes. To date, none of the available antidiabetic drugs promotes the maintenance of a functional mass of endogenous beta-cells, revealing an unmet medical need. Dysfunction and apoptotic death of beta-cells occur, in particular, through the activation of intracellular protein kinases. In recent years, protein kinases have become highly studied targets of the pharmaceutical industry for drug development. A number of drugs that inhibit protein kinases have been approved for the treatment of cancers. The question of whether safe drugs that inhibit protein kinase activity can be developed and used to protect the function and survival of beta-cells in diabetes is still unresolved. This review presents arguments suggesting that several protein kinases in beta-cells may represent targets of interest for the development of drugs to treat diabetes.
摘要：
糖尿病的患病率在世界范围内不断增加。胰腺β细胞的大量死亡导致1型糖尿病。β细胞功能和质量的进行性丧失是2型糖尿病的特征。迄今为止,没有可用的抗糖尿病药物促进内源性β细胞的功能质量的维持，揭示了未满足的医疗需求。β细胞发生功能障碍和凋亡性死亡，特别是,通过激活细胞内蛋白激酶。近年来,蛋白激酶已成为制药工业高度研究的药物开发目标。许多抑制蛋白激酶的药物已被批准用于治疗癌症。是否可以开发出抑制蛋白激酶活性的安全药物并用于保护糖尿病中β细胞的功能和存活的问题仍未解决。这篇评论提出的论点表明，β细胞中的几种蛋白激酶可能代表开发治疗糖尿病药物的目标。
