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RESEARCH PRODUCT
Mitochondria and T2D: Role of Autophagy, ER Stress, and Inflammasome.
Jordi MuntanéVictor M. VictorRubén Díaz-rúaNadezda ApostolovaMilagros Rochasubject
autophagyMitochondrial DiseasesInflammasomesEndocrinology Diabetes and Metabolism030209 endocrinology & metabolismMitochondrionmedicine.disease_causeInflammasome03 medical and health sciences0302 clinical medicineEndocrinologyinflammasomemedicineAutophagyAnimalsHumansbusiness.industryEndoplasmic reticulumAutophagyMolecular pathogenesisInflammasomeType 2 diabetesEndoplasmic Reticulum StressCell biologyMitochondriamitochondriaCrosstalk (biology)Oxidative StressDiabetes Mellitus Type 2Unfolded protein responsetype 2 diabetesbusinessOxidative stressmedicine.drugdescription
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.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2020-10-01 | Trends in endocrinology and metabolism: TEM |