β-Cell Autophagy in Diabetes Pathogenesis

被引:99
作者
Marasco, Michelle R. [1 ]
Linnemann, Amelia K. [1 ,2 ,3 ,4 ]
机构
[1] Indiana Univ Sch Med, Dept Pediat, Indianapolis, IN 46202 USA
[2] Indiana Univ Sch Med, Dept Biochem & Mol Biol, Indianapolis, IN 46202 USA
[3] Indiana Univ Sch Med, Dept Cellular & Integrat Physiol, Indianapolis, IN 46202 USA
[4] Indiana Univ Sch Med, Ctr Diabet & Metab Dis, Indianapolis, IN 46202 USA
关键词
ENDOPLASMIC-RETICULUM STRESS; RAPAMYCIN INDUCES AUTOPHAGY; PRO-INFLAMMATORY CYTOKINES; TRANSCRIPTION FACTOR NRF2; FREE FATTY-ACIDS; INSULIN-SECRETION; OXIDATIVE STRESS; MAMMALIAN AUTOPHAGY; IN-VITRO; APOPTOSIS;
D O I
10.1210/en.2017-03273
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Nearly 100 years have passed since Frederick Banting and Charles Best first discovered and purified insulin. Their discovery and subsequent improvements revolutionized the treatment of diabetes, and the field continues to move at an ever-faster pace with respect to unique treatments for both type 1 and type 2 diabetes. Despite these advances, we still do not fully understand howapoptosis of the insulin-producing beta-cells is triggered, presenting a challenge in the development of preventative measures. In recent years, the process of autophagy has generated substantial interest in this realm due to discoveries highlighting its clear role in the maintenance of cellular homeostasis. As a result, the number of studies focused on islet and beta-cell autophagy has increased substantially in recent years. In this review, we will discuss what is currently known regarding the role of beta-cell autophagy in type 1 and type 2 diabetes pathogenesis, with an emphasis on new and exciting developments over the past 5 years. Further, we will discuss how these discoveries might be translated into unique treatments in the coming years.
引用
收藏
页码:2127 / 2141
页数:15
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