Purpose of review: Multiple pathogenic mechanisms contribute to the development of diabetic cardiopathy, including intramyocardial inflammation, cardiac fibrosis, abnormal intracellular Ca handling, microangiopathy and endothelial dysfunction. Moreover, the cardiac kallikrein-kinin system is thought to be altered under diabetic conditions and an improvement of this peptide system, e.g. by gene therapeutic approaches, has also been associated with an amelioration of the diabetic heart. In this review, we will discuss the hypothesis that the stimulation of the kallikrein-kinin system could be a promising target for the treatment of diabetic cardiopathy.
Recent findings: The kallikrein-kinin system has cardioprotective properties, which may be particularly important under diabetic conditions. For example, its potential for endothelium-dependent vasodilation, and for improvement of glucose transport and utilization, make bradykinin an important mediator for reducing the consequences of diabetes-related oxidative stress on both the myocardium and vessels.
Summary: The different synergistic cardioprotective effects of the kallikrein-kinin system in the diabetic heart suggest that the stimulation of the kallikrein-kinin system might open new avenues for the treatment of diabetic cardiopathy.