Invited Review ArticleNuclear Calcium in Cardiac MyocytesLjubojevic, Senka PhD*; Bers, Donald M. PhD†Author Information *Department of Cardiology, Medical University of Graz, Graz, Austria; and †Department of Pharmacology, University of California Davis, Davis, CA. Reprints: Donald M. Bers, PhD, Department of Pharmacology, University of California Davis, 451 Health Sciences Drive, Davis, CA 95616 (e-mail: firstname.lastname@example.org). Supported by the Austrian Science Fund, FWF “Hertha-Firnberg Program” T-607 (S. Ljubojevic) and National Institutes of Health P01-HL080101 (D. M. Bers). The authors report no conflicts of interest. Received August 06, 2014 Accepted October 02, 2014 Journal of Cardiovascular Pharmacology: March 2015 - Volume 65 - Issue 3 - p 211-217 doi: 10.1097/FJC.0000000000000174 Buy Metrics Abstract Abstract: Calcium (Ca2+) is a universal second messenger involved in the regulation of various cellular processes, including electrical signaling, contraction, secretion, memory, gene transcription, and cell death. In heart, Ca2+ governs cardiomyocyte contraction, is central in electrophysiological properties, and controls major signaling pathway implicated in gene transcription. How cardiomyocytes decode Ca2+ signal to regulate gene expression without interfering with, or being controlled by, “contractile” Ca2+ that floods the entire cytosol during each heartbeat is still elusive. In this review, we summarize recent findings on nuclear Ca2+ regulation and its downstream signaling in cardiomyocytes. We will address difficulties in reliable quantification of nuclear Ca2+ fluxes and discuss its role in the development and progression of cardiac hypertrophy and heart failure. We also point out key open questions to stimulate future work. Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.