Diabetes mellitus is a metabolic disease caused by both genetic and environmental factors. The pathogenic mechanism(s) of diabetes are complex, and the complicated networks related to this disease involve distinct signaling pathways. Prolonged activation of the endoplasmic reticulum (ER) stress pathway known as the unfolded protein response (UPR) can lead to cell pathology and subsequent tissue dysfunction. There is now ample evidence that the UPR is chronically activated in many disease states including diabetes. Currently, discovery of potential modulators targeting these pathways has become a potent approach for antidiabetic drug lead compound development.

We invite investigators to contribute original research articles as well as review articles that will stimulate the continuing efforts to understand the molecular intricacies of ER stress and inflammation in diabetes and its vascular complications. We are particularly interested in articles describing the new insights into ER stress pathways by way of genetic, proteomic, biochemical, and molecular biology applications, advances in the identification of ER stress biomarkers in clinical, tissue culture, and animal models, and current concepts in therapeutic measures of diabetes beyond glucose control that would alleviate ER stress, inflammation, and oxidative stress. Potential topics include, but are not limited to:

• ER stress and UPR pathway
• ER stress in β-cell dysfunction
• ER stress and insulin resistance
• ER stress in diabetic nephropathy, diabetic retinopathy, and diabetic neuropathy
• ER stress in Type 1 diabetes
• Mediators of ER stress in atherosclerosis and metabolic syndrome
• Molecular interactions among ER stress, inflammation, and oxidative stress
• ER stress and islet amyloid alterations
• ER stress and autophagy
• Adaptive and apoptotic responses of ER stress
• ER stress, exercise and energy balance
• ER stress pathway and new targets for drug discovery
• Scope of traditional medicine as ER stress protectors

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