Endoplasmic Reticulum Stress-Induced Apoptosis and Autoimmunity in Diabetes

Author(s): Kathryn L. Lipson, Sonya G. Fonseca, Fumihiko Urano

Journal Name: Current Molecular Medicine

Volume 6 , Issue 1 , 2006

Become EABM
Become Reviewer


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 β-cells. Either a high level of ER stress or defective ER stress signaling in β-cells may cause an imbalance in ER homeostasis and lead to β-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.

Keywords: PKR-like ER kinase (PERK), Wolcott-Rallison Syndrome, EIF2AK3 gene, pro-apoptotic factors, JNK-inhibitory peptide

open access plus

Rights & PermissionsPrintExport Cite as

Article Details

Year: 2006
Page: [71 - 77]
Pages: 7
DOI: 10.2174/156652406775574613

Article Metrics

PDF: 32