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RESEARCH PRODUCT

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

subject

description

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. This research was funded by grants PI16/1083, PI16/0301, PI19/00838, PI19/00437, and CIBERehd CB06/04/0071 by Carlos III Health Institute and by the European Regional Development Fund (ERDF ‘A way to build Europe’); RTI2018- 096748-B-100 (Spanish Ministry of Science, Innovation and Universities), by PROMETEO2019/027 by Ministry of Education of the Valencian Regional Government; and by an unrestricted grant from Menarini S.A. M.R., and V.M. V are recipients of contracts from the Ministry of Health of the Valencian Regional Government and Carlos III Health Institute (CPII16/00037 and CES10/030, respectively).