Service of Endocrinology, University Hospital Doctor Peset, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Valencia, Spain; Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Madrid, Spain.
Department of Pharmacology, University of Valencia, Valencia, Spain.
Trends Endocrinol Metab. 2020 Oct;31(10):725-741. doi: 10.1016/j.tem.2020.03.004. Epub 2020 Apr 4.
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.
2 型糖尿病（T2D）是当前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，我们在扩展对受线粒体调节的信号事件的认识方面取得了巨大进展。然而，线粒体损伤、氧化应激、自噬、内质网（ER）应激和炎性小体激活之间的联系仍需阐明。有鉴于此，我们旨在对现有的文献进行综述，讨论 T2D 分子发病机制中，线粒体损伤、自噬、ER 应激和炎性小体之间复杂的串扰。
