title: Endoplasmic reticulum stress in beta cells and autoimmune diabetes.
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.
authors.affiliation: Department of Pediatrics, Washington University School of Medicine, St. Louis, MO 63110, USA.
authors.forename: Amy L
authors.initials: AL
authors.lastname: Clark
authors.affiliation: Department of Medicine, Division of Endocrinology, Metabolism, and Lipid Research, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. Electronic address: urano@wustl.edu.
authors.forename: Fumihiko
authors.initials: F
authors.lastname: Urano
mesh_terms: D000818:Animals; D015551:Autoimmunity; D002352:Carrier Proteins / Q000235:genetics / Q000378:metabolism*; D016207:Cytokines / Q000378:metabolism; D003922:Diabetes Mellitus, Type 1 / Q000276:immunology*; D059865:Endoplasmic Reticulum Stress; D006801:Humans; D056747:Immunomodulation; D007249:Inflammation; D018836:Inflammation Mediators / Q000378:metabolism; D050417:Insulin-Secreting Cells / Q000276:immunology*; D058990:Molecular Targeted Therapy
chemical_list: D002352:Carrier Proteins; D016207:Cytokines; D018836:Inflammation Mediators; C486715:TXNIP protein, human