Dilation of human atria: Increased diffusion restrictions for ADP,overexpression of hexokinase 2 and its coupling to oxidative phosphorylation in cardiomyocytes |
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| Authors: | Mart Roosimaa Taavi Põdramägi Lumme Kadaja Arno Ruusalepp Kalju Paju Raivo Puhke Margus Eimre Ehte Orlova Andres Piirsoo Nadežda Peet Frank N Gellerich Enn Seppet |
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| Institution: | 1. Institute of Biomedicine, Faculty of Medicine, University of Tartu, 19 Ravila Street, 50411 Tartu, Estonia;2. Institute of Exercise Biology and Physiotherapy Faculty of Exercise and Sport Sciences, University of Tartu, 14a Ravila Street, 50411 Tartu, Estonia;3. Department for Behavioral Neurology, Leibniz Institute for Neurobiology, Brennecke Str. 39118 Magdeburg, Germany;4. Department of Neurology, Otto von Guericke University of Leipziger Str. 44, Magdeburg, 39120 Magdeburg, Germany |
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| Abstract: | Cardiac energy metabolism with emphasis on mitochondria was addressed in atrial tissue from patients with overload-induced atrial dilation. Structural remodeling of dilated (D) atria manifested as intracellular accumulation of fibrillar aggregates, lipofuscin, signs of myolysis and autophagy. Despite impaired complex I dependent respiration and increased diffusion restriction for ADP, no changes regarding adenylate and creatine kinase occurred. We observed 7-fold overexpression of HK2 gene in D atria with concomitant 2-fold greater activation of mitochondrial oxygen consumption by glucose, which might represent an adaption to increased energy requirements and impaired mitochondrial function by effectively joining glycolysis and oxidative phosphorylation. |
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