Abstract
In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology begins a series of review articles on recent research advances into the mechanisms of diabetic vascular complications. The goal of this series is to review basic mechanisms by which diabetes accelerates vascular disease, an intense area of current interest. Research into diabetic vascular complications has received increased attention over the last 10 years as indicated by the number of articles published annually in ATVB that featured the term “diabetes” in the title, abstract, or text (Figure). Looking at the Figure, you might wonder what accounts both for the increase, and for the apparent lack of interest before this. This burst of activity was preceded by a greater realization that both type I and type II diabetes dramatically increase the risk for the development of macrovascular disease and its complications. The increase in published articles is also undoubtedly caused by many interdependent factors. First, it is now generally accepted that risk factors such as diabetes, hypertension, and hyperlipidemia have relatively acute effects on vascular cells to which their chronic adverse effects on vascular structure and function can be ascribed. For instance, in the case of diabetes, this principle is based on results from short-term cellular and physiological models in which vascular or blood cells in both animal models and in vitro are exposed to elevated concentrations of glucose for relatively brief periods of time. These are reasonably easy experiments to do, and bolstered by the fact that elevated …
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