Ischemic heart disease is one of the major causes of death worldwide. Ischemia is a condition in which blood flow of the myocardium declines, leading to cardiomyocyte death. However, reperfusion of ischemic regions decreases the rate of mortality, but it can also cause later complications. In a clinical setting, ischemic heart disease is always coincident with other co-morbidities such as diabetes. The risk of heart disease increases 2-3 times in diabetic patients. Apoptosis is considered to be one of the main pathophysiological mechanisms of myocardial ischemia-reperfusion injury. Diabetes can disrupt the anti-apoptotic intracellular signaling cascades involved in myocardial protection. Therefore, targeting these changes may be an effective cardioprotective approach in the diabetic myocardium against ischemia-reperfusion injury. In this article, we review the interaction of diabetes with the pathophysiology of myocardial ischemia-reperfusion injury, focusing on the contribution of apoptosis in this context, and then discuss the alterations of pro-apoptotic or anti-apoptotic pathways probably responsible for the loss of cardioprotection in diabetes.

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Sepsis is defined as a life-threatening organ failure due to dysregulated host response to infection. Despite current advances in our knowledge about sepsis, it is still considered as a major global health challenge. Myocardial dysfunction is a well-defined manifestation of sepsis which is related to worse outcomes in septic patients. Given that the heart is a mitochondria-rich organ and the normal function of mitochondria is essential for successful modulation of septic response, the contribution of mitochondrial damage in sepsis-related myocardial dysfunction has attracted the attention of many scientists. It is widely accepted that mitochondrial damage is involved in sepsis-related myocardial dysfunction; however, effective and potential treatment modalities in clinical setting are still lacking. Mitochondrial-based therapies are potential approaches in sepsis treatment. Although various therapeutic strategies have been used for mitochondrial function improvement, their effects are limited when mitochondria undergo irreversible alterations under septic challenge. Therefore, application of more effective approaches such as mitochondrial transplantation has been suggested. This review highlights the crucial role of mitochondrial damage in sepsis-related myocardial dysfunction, then provides an overview on mitochondrial-based therapies and current approaches to mitochondrial transplantation as a novel strategy, and proposes future directions for more researches in this field.

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