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UNCOUPLING PROTEIN DOWNREGULATION IN DOXORUBICIN INDUCED HEART FAILURE IMPROVES MITOCHONDRIAL COUPLING BUT INCREASES REACTIVE OXYGEN SPECIES GENERATION

机译:在多肠蛋白诱导的心力衰竭中下调的解耦蛋白质改善了线粒体偶联但增加了活性氧物种

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摘要

PURPOSEDoxorubicin-based chemotherapy is limited by the development of dose-dependent left ventricular dysfunction and congestive heart failure caused by reactive oxygen species (ROS). Uncoupling proteins (UCP) can inhibit mitochondrial ROS production as well as decrease myocyte damage from exogenous ROS. Prior studies have shown that cardiac UCP2 and UCP3 mRNA expression is decreased with acute doxorubicin treatment. However, the expression of UCP protein in hearts with doxorubicin cardiotoxicity and the resultant changes in mitochondrial function and oxidant stress have not been determined.

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