Interestingly, intracellular sodium concentration is increased in cardiomyocytes derived from diabetic hearts [110, 111]; this perturbation may compromise the capacity of mitochondria to generate ATP and reduce the generation of reactive oxygen species [112, 113]. It is therefore noteworthy that SIRT1/AMPK signaling modulates the activity of transporters so as to promote sodium efflux out of cells [49, 114,115,116]; the resulting decrease in intracellular sodium concentrations improves mitochondrial function and antioxidant defense mechanisms, thereby preventing cell death [112]. Interestingly, SGLT2 inhibitors have been shown to decrease intracellular sodium concentration in cardiomyocytes [117]. Although this finding has been attributed to an effect on sodium-hydrogen exchange in the heart, an effect of SGLT2 inhibitors on the exchanger has yet to be demonstrated. Instead, the effect of these drugs on cytosolic sodium may possibly be the result of AMPK/SIRT1 signaling.
exchange of hearts nr walker epub 23
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