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.
Oxidative stress, mitochondrial dysfunction, and type 2 diabetes are closely interconnected.Mitochondrial impairment characteristic for type 2 diabetes is related to changes in the autophagic process, endoplasmic reticulum stress, and inflammation.A new understanding of the pathophysiological mechanisms by which mitochondrial dysfunction and ROS, as essential signaling molecules, relate to other molecular pathways, could help to identify novel therapeutic targets for the treatment of type 2 diabetes.The identification of key molecular targets for type 2 diabetes treatment can widen the pharmacological scope for clinical development.