Endoplasmic reticulum stress in beta-cells and development of diabetes
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Document Type
Journal ArticlePublication Date
2009-08-12Keywords
Cell DeathDiabetes Mellitus, Type 1
Diabetes Mellitus, Type 2
Endoplasmic Reticulum
Humans
Insulin-Secreting Cells
Membrane Proteins
Models, Biological
Signal Transduction
Stress, Physiological
Unfolded Protein Response
Wolfram Syndrome
Genetics and Genomics
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Show full item recordAbstract
The endoplasmic reticulum (ER) is a cellular compartment responsible for multiple important cellular functions including the biosynthesis and folding of newly synthesized proteins destined for secretion, such as insulin. A myriad of pathological and physiological factors perturb ER function and cause dysregulation of ER homeostasis, leading to ER stress. ER stress elicits a signaling cascade to mitigate stress, the unfolded protein response (UPR). As long as the UPR can relieve stress, cells can produce the proper amount of proteins and maintain ER homeostasis. If the UPR, however, fails to maintain ER homeostasis, cells will undergo apoptosis. Activation of the UPR is critical to the survival of insulin-producing pancreatic beta-cells with high secretory protein production. Any disruption of ER homeostasis in beta-cells can lead to cell death and contribute to the pathogenesis of diabetes. There are several models of ER-stress-mediated diabetes. In this review, we outline the underlying molecular mechanisms of ER-stress-mediated beta-cell dysfunction and death during the progression of diabetes.Source
Curr Opin Pharmacol. 2009 Dec;9(6):763-70. Epub 2009 Aug 6. Link to article on publisher's siteDOI
10.1016/j.coph.2009.07.003Permanent Link to this Item
http://hdl.handle.net/20.500.14038/44090PubMed ID
19665428Related Resources
Link to Article in PubMedae974a485f413a2113503eed53cd6c53
10.1016/j.coph.2009.07.003