Dilation of human atria: Increased diffusion restrictions for ADP, overexpression of hexokinase 2 and its coupling to oxidative phosphorylation in cardiomyocytes

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.

► This study addressed the structural alterations in dilated human right atria.
► Mitochondrial function was assessed in permeabilized by saponin myocardial fibres.
► Suppressed apparent affinity of mitochondria to ADP in regulation of OXPHOS was revealed.
► Increased expression of hexokinase 2 coupled to OXPHOS was detected.
► Functional changes observed are related to structural remodeling of atria.