Endoplasmic Reticulum Stress-Induced Apoptosis and Autoimmunity in Diabetes

Title: Endoplasmic Reticulum Stress-Induced Apoptosis and Autoimmunity in Diabetes

Volume: 6 Issue: 1

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

Affiliation:

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

Abstract: 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.

Cite this article as:

Lipson L. Kathryn, Fonseca G. Sonya and Urano Fumihiko, Endoplasmic Reticulum Stress-Induced Apoptosis and Autoimmunity in Diabetes, Current Molecular Medicine 2006; 6 (1) . https://dx.doi.org/10.2174/156652406775574613