We believe that this approach may be applied both for systems biology research and, potentially, for quality control to accompany the development of novel stem cell-based therapies. Coronary GSK1016790A collateral growth is a physiological adaptive response to transient and repetitive occlusion of major coronary arteries in which small arterioles with minimal to no blood flow remodel into larger conduit arteries capable of supplying adequate perfusion to tissue distal to the site of occlusion. Transient repetitive coronary artery occlusion and resultant myocardial ischemia stimulate coronary collateral growth in healthy humans and normal animals. Clinically, patients with stable angina have decreased incidence of fatal myocardial infarction, which is associated with better developed collateral networks. In addition, well-developed collateral networks seem to promote long term patency of coronary bypass grafts. However, this normal physiological response is impaired in patients with type II TC-I 2014 diabetes and the metabolic syndrome. Graft closure, and consequent need for revascularization, is a significant problem in type II diabetic and metabolic syndrome patients. Therefore, the ability to reliably and reproducibly mimic transient, repetitive coronary artery ischemia in animal models is critical to the development of therapies to restore coronary collateral development in type II diabetes and the metabolic syndrome. Like in human metabolic syndrome, coronary collateral growth has been shown to be impaired in most animal models of the metabolic syndrome. However, normal collateral development has been reported in a swine model of the metabolic syndrome. The most obvious difference in the swine model is that this was a model of progressive chronic ischemia whereas the other animal models used transient, repetitive coronary artery occlusion to stimulate collateral development, which mimics the pathophysiology of the human. Since the exact timing and duration of coronary occlusions has been associated with the extent of collateral growth, the difference between these two methods of inducing coronary occlusion is a likely explanation for the different outcomes between the models and emphasizes the necessity of using transient and repetitive coronary occlusion models vs. progressive occlusion when studying coronary collateral development.