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Current Molecular Medicine

Volume 6 Issue 1
ISSN: 1566-5240
eISSN: 1875-5666

 

   All Titles

  Endoplasmic Reticulum Stress-Induced Apoptosis and Autoimmunity in Diabetes
  pp.71-77 (7) Authors: Kathryn L. Lipson, Sonya G. Fonseca, Fumihiko Urano
 
 
      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.

 
  Keywords: PKR-like ER kinase (PERK), Wolcott-Rallison Syndrome, EIF2AK3 gene, pro-apoptotic factors, JNK-inhibitory peptide
  Affiliation: Program in Gene Function and Expression, University of Massachusetts Medical School,Worcester, MA 01605-2324, USA.
 
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