Journal
AUTOPHAGY
Volume 7, Issue 1, Pages 2-11Publisher
TAYLOR & FRANCIS INC
DOI: 10.4161/auto.7.1.13044
Keywords
autophagy; diabetes mellitus; diabetes complications; oxidative stress; mitochondria dysfunction; autoimmunity
Categories
Funding
- ANPCyT [PICT 20555]
- CONICET [PIP 1607]
- UBA [M076]
- Buenos Aires, Argentina
- European Community [N. 115005]
- National Institutes of Health [R01-056997, R01-052387, M01-RR-00042, ULIRR024986]
- NATIONAL CENTER FOR RESEARCH RESOURCES [M01RR000042] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK053456] Funding Source: NIH RePORTER
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An emerging body of evidence supports a role for autophagy in the pathophysiology of type 1 and type 2 diabetes mellitus. Persistent high concentrations of glucose lead to imbalances in the antioxidant capacity within the cell resulting in oxidative stress-mediated injury in both disorders. An anticipated consequence of impaired autophagy is the accumulation of dysfunctional organelles such as mitochondria within the cell. Mitochondria are the primary site of the production of reactive oxygen species (ROS), and an imbalance in ROS production relative to the cytoprotective action of autophagy may lead to the accumulation of ROS. Impaired mitochondrial function associated with increased ROS levels have been proposed as mechanisms contributing to insulin resistance. In this article we review and interpret the literature that implicates a role for autophagy in the pathophysiology of type 1 and type 2 diabetes mellitus as it applies to beta-cell dysfunction, and more broadly to organ systems involved in complications of diabetes including the cardiovascular, renal and nervous systems.
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