Micro- and macrovascular complications are commonly seen in diabetic patients and en-dothelial dysfunction contributes to the development and progression of the complications. Abnormal functions in endothelial cells lead to the increase in vascular tension and atheroscle-rosis, followed by systemic hypertension as well as increased incidence of ischemia and stroke in diabetic patients. Mitochondria are organelles serving as a source of energy production and as regulators of cell survival (e.g., apoptosis and cell development) and ion homeostasis (e.g., H +, Ca 2+). Endothelial mitochondria are mainly responsible for generation of reactive oxy-gen species (ROS) and maintaining the Ca 2+ concentration in the cytosol. There is increasing evidence that mitochondrial morphological and functional changes are implicated in vascular endothelial dysfunction. Enhanced mitochondrial ission and/or attenuated fusion lead to mi-tochondrial fragmentation and disrupt the endothelial physiological function. Abnormal mito-chondrial biogenesis and disturbance of mitochondrial autophagy increase the accumulation of damaged mitochondria, such as irreversibly depolarized or leaky mitochondria, and facilitate cell death. Augmented mitochondrial ROS production and Ca 2+ overload in mitochondria not only cause the maladaptive effect on the endothelial function, but also are potentially detrimen-tal to cell survival. In this article, we review the physiological and pathophysiological role of mitochondria in endothelial function with special focus on diabetes.
- Fission and fusion
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