Invited Review ArticlemAKAP—A Master Scaffold for Cardiac RemodelingPassariello, Catherine L. PhD*; Li, Jinliang PhD*; Dodge-Kafka, Kimberly PhD†; Kapiloff, Michael S. MD, PhD*Author Information *Cardiac Signal Transduction and Cellular Biology Laboratory, Interdisciplinary Stem Cell Institute, Departments of Pediatrics and Medicine, Leonard M. Miller School of Medicine, University of Miami, Miami, FL; and †Calhoun Center for Cardiology, University of Connecticut Health Center, Farmington, CT. Reprints: Michael S. Kapiloff, MD, PhD, Cardiac Signal Transduction and Cellular Biology Laboratory, Interdisciplinary Stem Cell Institute, University of Miami Miller School of Medicine, R198, P.O. Box 016960, Miami, FL 33101 (e-mail: email@example.com). Supported by grants from the NIH (R01 HL075398—M.S.K.) and (F32 HL117537—C.L.P.) and the Florida Department of Health James and Esther King Biomedical Research Program (4KB08—M.S.K.). The authors are co-inventors of intellectual property concerning the use of mAKAP and RSK3 related inhibitors for the treatment of heart disease, for which a patent is pending and which may yield future royalties to both the authors and the University of Miami. This patent is currently assigned to Anchored RSK3 Inhibitors, LLC., in which M.S. Kapiloff is a corporate officer and holds equity. Received July 29, 2014 Accepted December 03, 2014 Journal of Cardiovascular Pharmacology: March 2015 - Volume 65 - Issue 3 - p 218-225 doi: 10.1097/FJC.0000000000000206 Buy Metrics Abstract Abstract: Cardiac remodeling is regulated by an extensive intracellular signal transduction network. Each of the many signaling pathways in this network contributes uniquely to the control of cellular adaptation. In the last few years, it has become apparent that multimolecular signaling complexes or “signalosomes” are important for fidelity in intracellular signaling and for mediating crosstalk between the different signaling pathways. These complexes integrate upstream signals and control downstream effectors. In the cardiac myocyte, the protein mAKAPβ serves as a scaffold for a large signalosome that is responsive to cAMP, calcium, hypoxia, and mitogen-activated protein kinase signaling. The main function of mAKAPβ signalosomes is to modulate stress-related gene expression regulated by the transcription factors NFATc, MEF2, and HIF-1α and type II histone deacetylases that control pathological cardiac hypertrophy. Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.