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Diabetologists have been well aware since the seminal work of Himsworth (1) in the 1930s that type 2 (insulin resistant) and type 1 (insulin deficient) diabetes were distinct entities with different pathophysiological bases. They have been aware for some time that type 2 diabetes is associated with resistance of tissues such as muscle and liver to the biological effects of insulin. Furthermore, they knew that type 2 diabetes per se and insulin resistance could both predispose to an increased risk of premature coronary artery disease and particularly the premature occurrence of myocardial infarction (MI). By contrast, cardiologists came to embrace these concepts only slowly. It was not until approximately 1999 (2) that the major organizations that represented them consistently designated type 2 diabetes as a risk factor for coronary artery disease. It was against this backdrop that we and others sought to identify pathophysiological determinants that were both manifestations of type 2 diabetes and determinants of acceleration of coronary artery disease and precipitation of MI. Because type 2 diabetes is the predominant form, comprising more than 90% of patients with diabetes, and because its association with premature coronary artery disease is particularly well established, type 2 diabetes is the focus of this article and was the focus of the journey from the bench to the bedside that it addresses. Because we were graciously invited to describe our particular journey, we have emphasized references to our own work.We and others have been interested in the fibrinolytic system in relation to the pathogenesis of coronary artery disease and precipitation of MI (3–5). Fibrinolysis in blood is mediated by activation of plasminogen activators, particularly tissue-type plasminogen activator (t-PA), that can be elaborated from endothelial cells in association with intravascular thrombosis (Fig. 1). t-PA is a serine protease. When it is …

PAI-1 and Diabetes: A Journey From the Bench to the Bedside