Mitochondria and T2D: Role of Autophagy, ER Stress, and Inflammasome

Trends Endocrinol Metab. 2020 Oct;31(10):725-741. doi: 10.1016/j.tem.2020.03.004. Epub 2020 Apr 4.

Abstract

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.

Keywords: autophagy; endoplasmic reticulum stress; inflammasome; mitochondria; oxidative stress; type 2 diabetes.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Autophagy* / physiology
  • Diabetes Mellitus, Type 2* / immunology
  • Diabetes Mellitus, Type 2* / metabolism
  • Endoplasmic Reticulum Stress* / physiology
  • Humans
  • Inflammasomes* / immunology
  • Inflammasomes* / metabolism
  • Mitochondrial Diseases* / immunology
  • Mitochondrial Diseases* / metabolism
  • Oxidative Stress* / physiology

Substances

  • Inflammasomes