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Experimental Diabetes Research
Volume 2012, Article ID 827971, 12 pages
Review Article

Endoplasmic Reticulum Stress and Diabetic Cardiomyopathy

1Department of Clinical Laboratory at the First Bethune Hospital, Jilin University, Changchun 130021, China
2Department of Pediatrics at the First Bethune Hospital, Jilin University, Changchun 130021, China
3Department of Pediatrics, University of Louisville, Louisville 40202, KY, USA

Received 16 July 2011; Revised 6 September 2011; Accepted 7 September 2011

Academic Editor: In-Kyu Lee

Copyright © 2012 Jiancheng Xu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The endoplasmic reticulum (ER) is an organelle entrusted with lipid synthesis, calcium homeostasis, protein folding, and maturation. Perturbation of ER-associated functions results in an evolutionarily conserved cell stress response, the unfolded protein response (UPR) that is also called ER stress. ER stress is aimed initially at compensating for damage but can eventually trigger cell death if ER stress is excessive or prolonged. Now the ER stress has been associated with numerous diseases. For instance, our recent studies have demonstrated the important role of ER stress in diabetes-induced cardiac cell death. It is known that apoptosis has been considered to play a critical role in diabetic cardiomyopathy. Therefore, this paper will summarize the information from the literature and our own studies to focus on the pathological role of ER stress in the development of diabetic cardiomyopathy. Improved understanding of the molecular mechanisms underlying UPR activation and ER-initiated apoptosis in diabetic cardiomyopathy will provide us with new targets for drug discovery and therapeutic intervention.