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      Calcium Signaling and Reactive Oxygen Species in Mitochondria

      1 , 1
      Circulation Research
      Ovid Technologies (Wolters Kluwer Health)

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          Abstract

          In heart failure, alterations of Na + and Ca 2+ handling, energetic deficit, and oxidative stress in cardiac myocytes are important pathophysiological hallmarks. Mitochondria are central to these processes because they are the main source for ATP, but also reactive oxygen species (ROS), and their function is critically controlled by Ca 2+ . During physiological variations of workload, mitochondrial Ca 2+ uptake is required to match energy supply to demand but also to keep the antioxidative capacity in a reduced state to prevent excessive emission of ROS. Mitochondria take up Ca 2+ via the mitochondrial Ca 2+ uniporter, which exists in a multiprotein complex whose molecular components were identified only recently. In heart failure, deterioration of cytosolic Ca 2+ and Na + handling hampers mitochondrial Ca 2+ uptake and the ensuing Krebs cycle–induced regeneration of the reduced forms of NADH (nicotinamide adenine dinucleotide) and NADPH (nicotinamide adenine dinucleotide phosphate), giving rise to energetic deficit and oxidative stress. ROS emission from mitochondria can trigger further ROS release from neighboring mitochondria termed ROS-induced ROS release, and cross talk between different ROS sources provides a spatially confined cellular network of redox signaling. Although low levels of ROS may serve physiological roles, higher levels interfere with excitation–contraction coupling, induce maladaptive cardiac remodeling through redox-sensitive kinases, and cell death through mitochondrial permeability transition. Targeting the dysregulated interplay between excitation–contraction coupling and mitochondrial energetics may ameliorate the progression of heart failure.

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          Author and article information

          Journal
          Circulation Research
          Circ Res
          Ovid Technologies (Wolters Kluwer Health)
          0009-7330
          1524-4571
          May 11 2018
          May 11 2018
          : 122
          : 10
          : 1460-1478
          Affiliations
          [1 ]From the Comprehensive Heart Failure Center, University Clinic Würzburg, Germany.
          Article
          10.1161/CIRCRESAHA.118.310082
          29748369
          0f3e9ee1-512f-46c8-9ba5-9d3b04ce12c2
          © 2018
          History

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