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• W2420374981 endingPage "853" @default.
• W2420374981 startingPage "848" @default.
• W2420374981 abstract "The excessive reactive oxygen species (ROS), produced by the electron leak in mitochondria of failing myocardium, play an important role in development and progression of heart failure (HF) and cardiac remodeling, which is associated with induction of myocyte hypertrophy and apoptosis and activation of matrix metalloproteinases. Furthermore, ROS can damage mitochondrial DNA(mtDNA), and thus lead to mitochondrial dysfunction and additional ROS generation. Recently, we found that the overexpression of mitochondrial transcription factor A (TFAM), which is essential for mtDNA transcription and replication, ameliorates cardiac remodeling and failure. Therefore, the regulation of mitochondrial oxidative stress or manipulation of TFAM protein may provide a novel therapeutic strategy of HF." @default.
• W2420374981 created "2016-06-24" @default.
• W2420374981 creator A5007114143 @default.
• W2420374981 creator A5091849037 @default.
• W2420374981 date "2006-05-01" @default.
• W2420374981 modified "2023-09-24" @default.
• W2420374981 title "Oxidative stress and heart failure" @default.
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