Production of Reactive Oxygen Species in the Diabetic Heart : Roles of Mitochondria and NADPH Oxidase

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  • Teshima Yasushi
    Department of Cardiology and Clinical Examination, Faculty of Medicine, Oita University
  • Takahashi Naohiko
    Department of Cardiology and Clinical Examination, Faculty of Medicine, Oita University
  • Nishio Satoru
    Department of Cardiology and Clinical Examination, Faculty of Medicine, Oita University
  • Saito Shotaro
    Department of Cardiology and Clinical Examination, Faculty of Medicine, Oita University
  • Kondo Hidekazu
    Department of Cardiology and Clinical Examination, Faculty of Medicine, Oita University
  • Fukui Akira
    Department of Cardiology and Clinical Examination, Faculty of Medicine, Oita University
  • Aoki Kouhei
    Department of Cardiology and Clinical Examination, Faculty of Medicine, Oita University
  • Yufu Kunio
    Department of Cardiology and Clinical Examination, Faculty of Medicine, Oita University
  • Nakagawa Mikiko
    Department of Cardiology and Clinical Examination, Faculty of Medicine, Oita University
  • Saikawa Tetsunori
    Department of Cardiology and Clinical Examination, Faculty of Medicine, Oita University

書誌事項

タイトル別名
  • Production of Reactive Oxygen Species in the Diabetic Heart
  • – Roles of Mitochondria and NADPH Oxidase –

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抄録

Reactive oxygen species (ROS) are the main facilitators of cardiovascular complications in diabetes mellitus (DM), and the ROS level is increased in cultured cells exposed to high glucose concentrations or in diabetic animal models. Emerging evidence shows that mitochondria and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase are dominant mechanisms of ROS production in the diabetic heart. Hyperpolarization of the mitochondrial inner membrane potentials and impaired mitochondrial function promote ROS production in the mitochondria of the diabetic heart. Uncoupling proteins are upregulated and may reduce the ROS level by depolarizing the mitochondrial inner membrane potential. NADPH oxidase is another major site of ROS production and its contribution to DM-induced ROS increase has been elucidated not only in vascular smooth muscle cells and endothelial cells, but also in cardiomyocytes. Protein kinase C, angiotensin II, and advanced glycation endproducts (AGEs)/receptor for AGEs can activate NADPH oxidase. Increased intracellular calcium level mediated via the Na+-H+ exchanger and subsequent activation of Ca2+/calmodulin-dependent protein kinase II may also activate NADPH oxidase. This review presents the current understanding of the mechanisms of ROS production, focusing especially on the roles of mitochondria and NADPH oxidase.  (Circ J 2014; 78: 300–306)<br>

収録刊行物

  • Circulation Journal

    Circulation Journal 78 (2), 300-306, 2014

    一般社団法人 日本循環器学会

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