We are analyzing https://link.springer.com/article/10.1007/s10534-012-9579-x.

Title:
Mitochondrial calcium uniporter blocker prevents cardiac mitochondrial dysfunction induced by iron overload in thalassemic mice | BioMetals
Description:
Iron-overload induced cardiomyopathy is a major cause of morbidity and mortality in thalassemic patients. Previous studies suggest that cardiac mitochondrial dysfunction may be involved in the pathogenesis of cardiomyopathy in thalassemia. We tested the hypothesis that iron overload causes dysfunction of cardiac mitochondria isolated from thalassemic mice. Cardiac mitochondria were isolated from the heart tissue of genetically-altered, β-thalassemic mice (HT) and adult wild-type mice (WT). Ferrous iron (Fe2+) at various concentrations (0–5 μg/ml) was applied to induce iron toxicity. Pharmacological interventions, facilitated by mitochondrial permeability transition pore (mPTP) blocker, CsA, and mitochondrial Ca2+ uniporter (MCU) blocker, Ru360, were used to study their respective effects on cardiac mitochondrial dysfunction. Cardiac mitochondrial ROS production, mitochondrial membrane potential changes, and mitochondrial swelling were determined. Iron overload caused increased ROS production, mitochondrial depolarization, and mitochondrial swelling in a dose-dependent manner in WT and HT cardiac mitochondria. CsA decreased only ROS production in WT and HT cardiac mitochondria, whereas Ru360 completely prevented the development of cardiac mitochondrial dysfunction by decreasing ROS, mitochondrial depolarization, and swelling in both WT and HT cardiac mitochondria. Ru360, an MCU blocker, provides protective effects by preventing ROS production and mitochondrial depolarization as well as attenuating mitochondrial swelling caused by Fe2+ overload. These findings indicate that the MCU could be a major portal for Fe2+ entry into cardiac mitochondria. Therefore, blocking MCU may be an effective therapy to prevent iron-overload induced cardiac mitochondrial dysfunction in patients with thalassemia.
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Keywords {🔍}

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Topics {✒️}

calcium-induced mitochondrial dysfunction month download article/chapter mitochondrial calcium uniporter t-type calcium channel cardiac mitochondrial dysfunction adult wild-type mice common beta0-thalassemia mutation mitochondrial ca2+ uniporter free radical-mediated mechanism article biometals aims author information authors mitochondrial calcium channels siriporn chattipakorn mitochondrial permeability transition humanized mouse model rat cardiac tissue cardiac mitochondria isolated ht cardiac mitochondria full article pdf author correspondence nipon chattipakorn chronic iron overload cardiac hypertrophy mechanism mitochondrial iron trafficking mitochondrial dysfunction iron overload cardiomyopathy iron-overload cardiomyopathy permeability transition pore mitochondrial ion channels privacy choices/manage cookies mitochondrial dna damage hbe/beta-thalassemia mcu blocker related subjects preventing ros production nonsynaptic mitochondria demonstrate mitochondrial membrane potential check access instant access mitochondrial ca2+ uptake cardiac mitochondria iron status assessment redox dependent mechanism article kumfu european economic area previous studies suggest dose-dependent manner energy-dependent accumulation mammalian iron metabolism heart rate variability

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         description:Iron-overload induced cardiomyopathy is a major cause of morbidity and mortality in thalassemic patients. Previous studies suggest that cardiac mitochondrial dysfunction may be involved in the pathogenesis of cardiomyopathy in thalassemia. We tested the hypothesis that iron overload causes dysfunction of cardiac mitochondria isolated from thalassemic mice. Cardiac mitochondria were isolated from the heart tissue of genetically-altered, β-thalassemic mice (HT) and adult wild-type mice (WT). Ferrous iron (Fe2+) at various concentrations (0–5 μg/ml) was applied to induce iron toxicity. Pharmacological interventions, facilitated by mitochondrial permeability transition pore (mPTP) blocker, CsA, and mitochondrial Ca2+ uniporter (MCU) blocker, Ru360, were used to study their respective effects on cardiac mitochondrial dysfunction. Cardiac mitochondrial ROS production, mitochondrial membrane potential changes, and mitochondrial swelling were determined. Iron overload caused increased ROS production, mitochondrial depolarization, and mitochondrial swelling in a dose-dependent manner in WT and HT cardiac mitochondria. CsA decreased only ROS production in WT and HT cardiac mitochondria, whereas Ru360 completely prevented the development of cardiac mitochondrial dysfunction by decreasing ROS, mitochondrial depolarization, and swelling in both WT and HT cardiac mitochondria. Ru360, an MCU blocker, provides protective effects by preventing ROS production and mitochondrial depolarization as well as attenuating mitochondrial swelling caused by Fe2+ overload. These findings indicate that the MCU could be a major portal for Fe2+ entry into cardiac mitochondria. Therefore, blocking MCU may be an effective therapy to prevent iron-overload induced cardiac mitochondrial dysfunction in patients with thalassemia.
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