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c-Jun氨基末端激酶在胰岛移植中的调控

Regulation of c-Jun NH-Terminal Kinase for Islet Transplantation.

作者信息

Noguchi Hirofumi

机构信息

Department of Regenerative Medicine, Graduate School of Medicine, University of the Ryukyus, Okinawa 903-0215, Japan.

出版信息

J Clin Med. 2019 Oct 23;8(11):1763. doi: 10.3390/jcm8111763.

Abstract

Islet transplantation has been demonstrated to provide superior glycemic control with reduced glucose lability and hypoglycemic events compared with standard insulin therapy. However, the insulin independence rate after islet transplantation from one donor pancreas has remained low. The low frequency of islet grafting is dependent on poor islet recovery from donors and early islet loss during the first hours following grafting. The reduction in islet mass during pancreas preservation, islet isolation, and islet transplantation leads to β-cell death by apoptosis and the prerecruitment of intracellular death signaling pathways, such as c-Jun NH-terminal kinase (JNK), which is one of the stress groups of mitogen-activated protein kinases (MAPKs). In this review, we show some of the most recent contributions to the advancement of knowledge of the JNK pathway and several possibilities for the treatment of diabetes using JNK inhibitors.

摘要

与标准胰岛素治疗相比,胰岛移植已被证明能提供更好的血糖控制,减少血糖波动和低血糖事件。然而,来自一个供体胰腺的胰岛移植后的胰岛素非依赖率仍然很低。胰岛移植的低频率取决于供体胰岛回收率低以及移植后最初几小时内胰岛的早期丢失。在胰腺保存、胰岛分离和胰岛移植过程中,胰岛质量的减少会导致β细胞通过凋亡死亡,并提前激活细胞内死亡信号通路,如c-Jun氨基末端激酶(JNK),它是丝裂原活化蛋白激酶(MAPK)应激组之一。在这篇综述中,我们展示了JNK通路知识进展的一些最新贡献以及使用JNK抑制剂治疗糖尿病的几种可能性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/300b/6912371/68c2dccd812b/jcm-08-01763-g001.jpg

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