Type 2 diabetes (T2D) is one of the main current threats to human health. Both T2D and its numerous clinical complications are related to mitochondrial dysfunction and oxidative stress. Over the past decade, great progress has been made in extending our knowledge about the signaling events regulated by mitochondria. However, the links among mitochondrial impairment, oxidative stress, autophagy, endoplasmic reticulum (ER) stress, and activation of the inflammasome still need to be clarified. In light of this deficit, we aim to provide a review of the existing literature concerning the complicated crosstalk between mitochondrial impairment, autophagy, ER stress, and the inflammasome in the molecular pathogenesis of T2D.

中文翻译：

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线粒体和 T2D：自噬、内质网应激和炎症小体的作用

2 型糖尿病 (T2D) 是当前对人类健康的主要威胁之一。T2D 及其众多临床并发症都与线粒体功能障碍和氧化应激有关。在过去的十年中，在扩展我们对线粒体调控的信号事件的认识方面取得了很大进展。然而，线粒体损伤、氧化应激、自噬、内质网 (ER) 应激和炎症小体激活之间的联系仍有待阐明。鉴于这一缺陷，我们旨在对现有文献进行综述，这些文献涉及线粒体损伤、自噬、内质网应激和 T2D 分子发病机制中炎性体之间的复杂串扰。