Patients with pre-existing type 2 diabetes have significantly impaired clinical outcomes following a cardiovascular event (e.g. ischemia), in comparison to otherwise ‘healthy’ individuals. We suggest that the type 2 diabetes heart undergoes molecular adaptations that subsequently increase cell death or reduce pro-survival mechanisms upon ischemia. We have also observed elevated controlled cell death (‘apoptosis’) in rodent myocardial models of T2DM that were not subjected to a cardiovascular event. Our overall aim therefore is to characterize these adaptations in diabetic hearts to determine the molecular ‘priming’ that results in poor outcomes in response to cardiovascular stress. Improving our understanding of the changes that characterise diabetic hearts provides a unique pathway for development of pharmacological intervention to improve cardiovascular outcomes for those suffering with type 2 diabetes.
Last updated12 July 2021