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Endoplasmic Reticulum Stress-Induced Apoptosis and Autoimmunity in Diabetes

[ Vol. 6 , Issue. 1 ]


Kathryn L. Lipson, Sonya G. Fonseca and Fumihiko Urano   Pages 71 - 77 ( 7 )


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.


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


Program in Gene Function and Expression, University of Massachusetts Medical School,Worcester, MA 01605-2324, USA.

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