In this issue, we selected two articles highlighted the link between stress signal and glycation.
The first article written by Dr. Christos Adamopoulos and Prof. Christina Piperi, Department of Biological Chemistry, Medical School, National and Kapodistrian University of Athens, Greece, summarized that high-AGE content diet causes endoplasmic reticulum (ER) dysfunction, referred to as ER stress, in brain, kidney, liver and pancreas, and thereby induces stress signal, unfolded protein response (UPR). The UPR pathway is known to regulate not only protein homeostasis, but also glucose and lipid metabolism. Thus, dietary AGEs may contribute to development and progression of metabolic diseases via the UPR activation that alters metabolic status in metabolic organs.
The second article written by Prof. Chih-Kang Chiang, Graduate Institute of Toxicology, College of Medicine, National Taiwan University, Taiwan, demonstrated the impact of pathogenic effect of AGEs on mesangial cell injury, which is one of the major phenotypic changes of diabetic nephropathy. AGEs induce ER stress in mesangial cells, and subsequently decrease mesangial cell viability associated with induction of apoptosis. Importantly, such AGEs-ER stress-mesangial cell apoptosis axis is regulated by autophagy. These findings suggest that the AGEs-induced autophagy mediated by ER stress may be a therapeutic target for prevention of mesangial cell damage and subsequent progression of diabetic nephropathy.
I deeply thank their great contributions to the IMARS Highlights. The IMARS Highlights editors always look forward to submission of your articles, comments to any kinds of issues published in IMARS Highlights and other glycation-related issues in the field of food and medical sciences.
Reiko Inagi, Ph.D.
Division of Chronic Kidney Disease Pathophysiology,
The University of Tokyo Graduate School of Medicine
email: [email protected]