Endoplasmic reticulum stress-induced apoptosis and auto-immunity in diabetes
Biochemistry & Molecular Pharmacology
Graduate School of Biomedical Sciences; Program in Gene Function and Expression
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.
DOI of Published Version
Curr Mol Med. 2006 Feb;6(1):71-7.
Current molecular medicine
Lipson KL, Fonseca SG, Urano F. (2006). Endoplasmic reticulum stress-induced apoptosis and auto-immunity in diabetes. GSBS Student Publications. https://doi.org/10.2174/156652406775574613. Retrieved from https://escholarship.umassmed.edu/gsbs_sp/770