Ca2+ is a key component of cardiomyocyte excitation-contraction (E-C) coupling. Ca2+-regulatory proteins regulate intracellular free Ca2+ concentrations and maintain intracellular Ca2+ homeostasis so it is very important for E-C coupling and for myocyte contractility [5]. The most important Ca2+-regulatory proteins include sarcoplasmic reticulum (SR) Ca2+-ATPase (SERCA2a), ryanodine receptor (RyR2, the cardiac isoform of RyR), sodiumcalcium exchanger (NCX), sarcolipin (SLN), and phospholamban (PLN) [5]. Abnormal parts of Ca2+-regulatory proteins in ventricular hypertrophy (LVH) are well established from animal models [6]. Few, if any, studies have examined these proteins in human LVH or RVH, due to a lack of tissue availability. Bartelds and colleagues have reported pressure load can induce different functional and molecular adaptations in the right ventricle (RV) from left ventricle (LV) [7]. In addition, it is important that the reported Ca2+-regulatory proteins changes have not been consistent among all animal models of LVH [8, 9]. Such discrepancies further emphasize that it is necessary to examine these proteins changes associated with RVH in the human heart, rather than generalizing from LVH of animal models. Furthermore, hypoxia is a severe pathophysiological condition that can induce RVH[10, 11] and can also alter the expression of Ca2+-regulatory proteins in hearts from animal models, however there is no evidence of this in the human heart [10, 12]. Therefore, research about the alteration of Ca2+-regulatory proteins in RVH with or without hypoxia will help to understand the cellular and molecular bases of RVH and hypoxia in the populations of children with CHD.
Ca2+-regulatory proteins regulate intracellular free Ca2+ concentrations and maintain intracellular Ca2+ homeostasis and thus have a very important role in the process of myocardial contraction and relaxation [5]. Hypoxia and hypertrophy are the most frequent pathophysiological consequence of CHD which can induce the alteration of parts of Ca2+-regulatory proteins and thus inhibit cardiac contractility [10, 12, 26]. The changes of RV are the key pathologic changes of CHD [27]. However, few studies have been performed to examine Ca2+-regulatory proteins in human RV during hypoxia and hypertrophy, due to a lack of tissue sources.
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