Article

Endoplasmic reticulum stress-induced apoptosis and auto-immunity in diabetes.

Program in Gene Function and Expression, University of Massachusetts Medical School, Worcester, 01605-2324, USA.
Current Molecular Medicine (Impact Factor: 4.2). 03/2006; 6(1):71-7. DOI: 10.2174/156652406775574613
Source: PubMed

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 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.

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