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Transcriptional Pathways and Potential Therapeutic Targets in the Regulation of Ncx1 Expression in Cardiac Hypertrophy and Failure

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Sodium Calcium Exchange: A Growing Spectrum of Pathophysiological Implications

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 961))

Abstract

Changes in cardiac gene expression contribute to the progression of heart failure by affecting cardiomyocyte growth, function, and survival. The Na+-Ca2+ exchanger gene (Ncx1) is upregulated in hypertrophy and is often found elevated in end-stage heart failure. Studies have shown that the change in its expression contributes to contractile dysfunction. Several transcriptional pathways mediate Ncx1 expression in pathological cardiac remodeling. Both α-adrenergic receptor (α-AR) and β-adrenergic receptor (β-AR) signaling can play a role in the regulation of calcium homeostasis in the cardiomyocyte, but chronic activation in periods of cardiac stress contributes to heart failure by mechanisms which include Ncx1 upregulation. Our studies have even demonstrated that NCX1 can directly act as a regulator of “activity-dependent signal transduction” mediating changes in its own expression. Finally, we present evidence that histone deacetylases (HDACs) and histone acetyltransferases (HATs) act as master regulators of Ncx1 expression. We show that many of the transcription factors regulating Ncx1 expression are important in cardiac development and also in the regulation of many other genes in the so-called fetal gene program, which are activated by pathological stimuli. Importantly, studies have revealed that the transcriptional network regulating Ncx1 expression is also mediating many of the other changes in genetic remodeling contributing to the development of cardiac dysfunction and revealed potential therapeutic targets for the treatment of hypertrophy and failure.

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Acknowledgements

This work was supported by NIH R01HL095696 (DRM) and NIH T32HL07260 (MSL, OC, and DK).

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  1. Division of Cardiology, Department of Medicine, Gazes Cardiac Research Institute, Medical University of South Carolina, 114 Doughty Street, 250773, Charleston, SC, 29425, USA

    Donald R. Menick, Mona S. Li, Olga Chernysh, Ludivine Renaud, Denise Kimbrough, Harinath Kasiganesan & Santhosh K. Mani

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  1. Donald R. Menick
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  1. Dipto. Neuroscienze e di, Università di Napoli Fac. Medicina e Chirurgia, Napoli, Italy

    Lucio Annunziato

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Menick, D.R. et al. (2013). Transcriptional Pathways and Potential Therapeutic Targets in the Regulation of Ncx1 Expression in Cardiac Hypertrophy and Failure. In: Annunziato, L. (eds) Sodium Calcium Exchange: A Growing Spectrum of Pathophysiological Implications. Advances in Experimental Medicine and Biology, vol 961. Springer, Boston, MA. https://doi.org/10.1007/978-1-4614-4756-6_11

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