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Interaction between Mitochondria and the Endoplasmic Reticulum: Implications for the Pathogenesis of Type 2 Diabetes Mellitus

机译:线粒体和内质网之间的相互作用:对2型糖尿病发病机制的影响。

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Mitochondrial dysfunction and endoplasmic reticulum (ER) stress are closely associated withβ-cell dysfunction and peripheral insulin resistance. Thus, each of these factors contributes to the development of type 2 diabetes mellitus (DM). The accumulated evidence reveals structural and functional communications between mitochondria and the ER. It is now well established that ER stress causes apoptotic cell death by disturbing mitochondrial Ca2+homeostasis. In addition, recent studies have shown that mitochondrial dysfunction causes ER stress. In this paper, we summarize the roles that mitochondrial dysfunction and ER stress play in the pathogenesis of type 2 DM. Structural and functional communications between mitochondria and the ER are also discussed. Finally, we focus on recent findings supporting the hypothesis that mitochondrial dysfunction and the subsequent induction of ER stress play important roles in the pathogenesis of type 2 DM.
机译:线粒体功能障碍和内质网应激与β细胞功能障碍和外周胰岛素抵抗密切相关。因此,这些因素中的每一个都有助于2型糖尿病(DM)的发展。积累的证据揭示了线粒体与内质网之间的结构和功能通讯。现在已经确定,ER应激会通过干扰线粒体Ca2 +稳态而导致凋亡性细胞死亡。此外,最近的研究表明,线粒体功能障碍会引起内质网应激。在本文中,我们总结了线粒体功能障碍和内质网应激在2型DM发病机理中的作用。还讨论了线粒体和ER之间的结构和功能通讯。最后,我们重点关注支持线粒体功能障碍和随后的ER应激在2型DM发病机理中起重要作用的假说的最新发现。

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