Endoplasmic reticulum stress-induced apoptosis and auto-immunity in diabetes
Graduate School of Biomedical Sciences; Program in Gene Function and Expression
Medical Subject Headings
*Apoptosis; Autoimmunity; Diabetes Mellitus; Endoplasmic Reticulum; Humans; Insulin-Secreting Cells
Life Sciences | Medicine and Health Sciences
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.
Rights and Permissions
Citation: Curr Mol Med. 2006 Feb;6(1):71-7.
Current molecular medicine
Lipson, Kathryn L.; Fonseca, Sonya G.; and Urano, Fumihiko, "Endoplasmic reticulum stress-induced apoptosis and auto-immunity in diabetes" (2006). GSBS Student Publications. 770.