Endoplasmic reticulum stress-induced apoptosis and auto-immunity in diabetes.
Increasing evidence suggests that stress signaling pathways emanating from the endoplasmic reticulum (ER) are important to the pathogenesis of both type 1 and type 2 diabetes. Recent observations indicate that ER stress signaling participates in maintaining the ER homeostasis of pancreatic beta-cells. Either a high level of ER stress or defective ER stress signaling in beta-cells may cause an imbalance in ER homeostasis and lead to beta-cell apoptosis and autoimmune response. In addition, it has been suggested that ER stress attributes to insulin resistance in patients with type 2 diabetes. It is necessary to study the relationship between ER stress and diabetes in order to develop new therapeutic approaches to diabetes based on drugs that block the ER stress-mediated cell-death pathway and insulin resistance.
Program in Gene Function and Expression, University of Massachusetts Medical School, Worcester, 01605-2324, USA.
Kathryn L
KL
Lipson
Sonya G
SG
Fonseca
Fumihiko
F
Urano
D017209:Apoptosis; D015551:Autoimmunity / Q000276:immunology*; D003920:Diabetes Mellitus / Q000276:immunology* / Q000473:pathology*; D004721:Endoplasmic Reticulum / Q000378:metabolism* / Q000473:pathology*; D006801:Humans; D050417:Insulin-Secreting Cells / Q000276:immunology / Q000473:pathology