The role of labile Zn and Zn-transporters in the pathophysiology of mitochondria dysfunction in cardiomyocytes.
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An important energy supplier of cardiomyocytes is mitochondria, similar to other mammalian cells. Studies have demonstrated that any defect in the normal processes controlled by mitochondria can lead to abnormal ROS production, thereby high oxidative stress as well as lack of ATP. Taken into consideration, the relationship between mitochondrial dysfunction and overproduction of ROS as well as the relation between increased ROS and high-level release of intracellular labile Zn, those bring into consideration the importance of the events related with those stimuli in cardiomyocytes responsible from cellular Zn-homeostasis and responsible Zn-transporters associated with the Zn-homeostasis and Zn-signaling. Zn-signaling, controlled by cellular Zn-homeostatic mechanisms, is regulated with intracellular labile Zn levels, which are controlled, especially, with the two Zn-transporter families; ZIPs and ZnTs. Our experimental studies in mammalian cardiomyocytes and human heart tissue showed that Zn-transporters localizes to mitochondria besides sarco(endo)plasmic reticulum and Golgi under physiological condition. The protein levels as well as functions of those transporters can re-distribute under pathological conditions, therefore, they can interplay among organelles in cardiomyocytes to adjust a proper intracellular labile Zn level. In the present review, we aimed to summarize the already known Zn-transporters localize to mitochondria and function to stabilize not only the cellular Zn level but also cellular oxidative stress status. In conclusion, one can propose that a detailed understanding of cellular Zn-homeostasis and Zn-signaling through mitochondria may emphasize the importance of new mitochondria-targeting agents for prevention and/or therapy of cardiovascular dysfunction in humans.
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