Abstract
The prevalence of diabetes continues to increase world-wide and is a leading cause of morbidity, mortality, and rapidly rising health care costs. Although strict glucose control combined with good pharmacological and non-pharmacologic interventions can increase diabetic patient life span, the frequency and mortality of myocardial ischemia and infarction remain drastically increased in diabetic patients. Therefore, more effective therapeutic approaches are urgently needed. Over the past 15 years, cellular repair of the injured adult heart has become the focus of a rapidly expanding broad spectrum of pre-clinical and clinical research. Recent clinical trials have achieved favorable initial endpoints with improvements in cardiac function and clinical symptoms following cellular therapy. Due to the increased risk of cardiac disease, cardiac regeneration may be one strategy to treat patients with diabetic cardiomyopathy and/or myocardial infarction. However, pre-clinical studies suggest that the diabetic myocardium may not be a favorable environment for the transplantation and survival of stem cells due to altered kinetics in cellular homing, survival, and in situ remodeling. Therefore, unique conditions in the diabetic myocardium will require novel solutions in order to increase the efficiency of cellular repair following ischemia and/or infarction. This review briefly summarizes some of the recent advances in cardiac regeneration in non-diabetic conditions and then provides an overview of some of the issues related to diabetes that must be addressed in the coming years.
Highlights
The prevalence of diabetes continues to increase world-wide and is a leading cause of morbidity, mortality, and rapidly rising health care costs
Eight weeks after myocardial infarction (MI), transplantation of fibroblasts stably transfected to express Stromal derived factor-1 (SDF-1) and increase the homing of CD117+ Mesenchymal stem cell (MSC) into the peri-infarct zone of syngeneic rat hearts resulted in greater left ventricular (LV) mass and better cardiac function, suggesting the important role of SDF-1 to induce MSCs homing to injured myocardium [53]
Possible strategies to prevent or reverse the negative diabetic effect on Stem cell (SC) and cardiac regenerative therapies Improvement of stem cell function impaired by diabetes The observation that hyperglycemic inhibition of the migration of Cardiac stem cell (CSC) is due to the suppression of Stem cell factor (SCF) expression via reduction in ERK1/2 and p38 MAPK phosphorylation may imply a possibility whether activation of ERK1/2 and p38 MAPK can be a tool to prevent diabetic suppression of myocardial SCF expression to attract the migration of CSCs to infarcted cardiac tissues
Summary
The prevalence of diabetes continues to increase world-wide and is a leading cause of morbidity, mortality, and rapidly rising health care costs. Eight weeks after MI, transplantation of fibroblasts stably transfected to express SDF-1 and increase the homing of CD117+ ( called c-kit+) MSCs into the peri-infarct zone of syngeneic rat hearts resulted in greater LV mass and better cardiac function, suggesting the important role of SDF-1 to induce MSCs homing to injured myocardium [53].
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