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- W2166134799 abstract "Autophagy functions to degrade and recycle intracellular proteins and damaged organelles, maintaining the normal cellular function. Autophagy has been shown to play an important role in regulating normal function of pancreatic β cells and insulin-target tissues, such as skeletal muscle, liver, and adipose tissue. Enhanced autophagy also acts as a protective mechanism against oxidative stress in these tissues. Altered autophagic activity has been implicated in the progression of obesity to type 2 diabetes through impaired β-cell function and development of insulin resistance. In this review, we outline the normal regulation of autophagy in β cells and insulin target tissues and explore the dysregulation of autophagy in diabetic animal models and human subjects with type 2 diabetes. Furthermore, we highlight the role of impaired autophagy in the pathophysiology of diabetic complications, including nephropathy and cardiomyopathy. Finally, we summarize how autophagy might be targeted as a therapeutic option in type 2 diabetes." @default.
- W2166134799 created "2016-06-24" @default.
- W2166134799 creator A5049045028 @default.
- W2166134799 creator A5056384996 @default.
- W2166134799 date "2015-04-01" @default.
- W2166134799 modified "2023-10-18" @default.
- W2166134799 title "Autophagy in Diabetes: β-Cell Dysfunction, Insulin Resistance, and Complications" @default.
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- W2166134799 doi "https://doi.org/10.1089/dna.2014.2755" @default.
- W2166134799 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25665094" @default.
- W2166134799 hasPublicationYear "2015" @default.
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