| Literature DB >> 27718448 |
Amy L Clark1, Fumihiko Urano2.
Abstract
Type 1 diabetes results from the autoimmune destruction of pancreatic β cells, leading to insulin deficiency and hyperglycemia. Although multiple attempts have been made to slow the autoimmune process using immunosuppressive or immunomodulatory agents, there are still no effective treatments that can delay or reverse the progression of type 1 diabetes in humans. Recent studies support endoplasmic reticulum (ER) as a novel target for preventing the initiation of the autoimmune reaction, propagation of inflammation, and β cell death in type 1 diabetes. This review highlights recent findings on ER stress in β cells and development of type 1 diabetes and introduces potential new treatments targeting the ER to combat this disorder. Copyright ÂEntities:
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Year: 2016 PMID: 27718448 PMCID: PMC5125892 DOI: 10.1016/j.coi.2016.09.006
Source DB: PubMed Journal: Curr Opin Immunol ISSN: 0952-7915 Impact factor: 7.486