Ai,, X., Curran,, J. W., Shannon,, T. R., Bers,, D. M., & Pogwizd,, S. M. (2005). Ca2+/calmodulin‐dependent protein kinase modulates cardiac ryanodine receptor phosphorylation and sarcoplasmic reticulum Ca2+ leak in heart failure. Circulation Research, 97, 1314–1322.
Ai,, X., & Pogwizd,, S. M. (2005). Connexin 43 downregulation and dephosphorylation in nonischemic heart failure is associated with enhanced colocalized protein phosphatase type 2A. Circulation Research, 96, 54–63.
Aistrup,, G. L., Shiferaw,, Y., Kapur,, S., Kadish,, A. H., & Wasserstrom,, J. A. (2009). Mechanisms underlying the formation and dynamics of subcellular calcium alternans in the intact rat heart. Circulation Research, 104, 639–649.
Akar,, F. G., & Rosenbaum,, D. S. (2003). Transmural electrophysiological heterogeneities underlying arrhythmogenesis in heart failure. Circulation Research, 93, 638–645.
Anderson,, M. E. (2007). Multiple downstream proarrhythmic targets for calmodulin kinase II: Moving beyond an ion channel‐centric focus. Cardiovascular Research, 73, 657–666.
Benjamin,, E. J., Blaha,, M. J., Chiuve,, S. E., Cushman,, M., Das,, S. R., Deo,, R., … American Heart Association Statistics C and Stroke Statistics S. (2017). Heart disease and stroke statistics‐2017 update: A report from the American Heart Association. Circulation, 135, e146–e603.
Bers,, D. M., & Grandi,, E. (2009). Calcium/calmodulin‐dependent kinase II regulation of cardiac ion channels. Journal of Cardiovascular Pharmacology, 54, 180–187.
Bers,, D. M., & Morotti,, S. (2014). Ca2+ current facilitation is CaMKII‐dependent and has arrhythmogenic consequences. Frontiers in Pharmacology, 5, 144.
Boulaksil,, M., Winckels,, S. K., Engelen,, M. A., Stein,, M., van Veen,, T. A., Jansen,, J. A., … van Rijen,, H. V. (2010). Heterogeneous Connexin43 distribution in heart failure is associated with dispersed conduction and enhanced susceptibility to ventricular arrhythmias. European Journal of Heart Failure, 12, 913–921.
Campbell,, S. G., Flaim,, S. N., Leem,, C. H., & McCulloch,, A. D. (2008). Mechanisms of transmurally varying myocyte electromechanics in an integrated computational model. Philosophical Transactions. Series A, Mathematical, Physical, and Engineering Science, 366, 3361–3380.
Campbell,, S. G., Lionetti,, F. V., Campbell,, K. S., & McCulloch,, A. D. (2010). Coupling of adjacent tropomyosins enhances cross‐bridge‐mediated cooperative activation in a Markov model of the cardiac thin filament. Biophysical Journal, 98, 2254–2264.
Chang,, S. N., Chang,, S. H., Yu,, C. C., Wu,, C. K., Lai,, L. P., Chiang,, F. T., … Tsai,, C. T. (2017). Renal denervation decreases susceptibility to arrhythmogenic cardiac alternans and ventricular arrhythmia in a rat model of post‐myocardial infarction heart failure. Journal of the American College of Cardiology Basic Transactions on Science, 2, 9.
Chelu,, M. G., Sarma,, S., Sood,, S., Wang,, S., van Oort,, R. J., Skapura,, D. G., … Wehrens,, X. H. (2009). Calmodulin kinase II‐mediated sarcoplasmic reticulum Ca2+ leak promotes atrial fibrillation in mice. The Journal of Clinical Investigation, 119, 1940–1951.
Christensen,, M. D., Dun,, W., Boyden,, P. A., Anderson,, M. E., Mohler,, P. J., & Hund,, T. J. (2009). Oxidized calmodulin kinase II regulates conduction following myocardial infarction: A computational analysis. PLoS Computational Biology, 5, e1000583.
Cooling,, M., Hunter,, P., & Crampin,, E. J. (2007). Modeling hypertrophic IP3 transients in the cardiac myocyte. Biophysical Journal, 93, 3421–3433.
Cooling,, M. T., Hunter,, P., & Crampin,, E. J. (2009). Sensitivity of NFAT cycling to cytosolic calcium concentration: Implications for hypertrophic signals in cardiac myocytes. Biophysical Journal, 96, 2095–2104.
Cortassa,, S., Aon,, M. A., O`Rourke,, B., Jacques,, R., Tseng,, H. J., Marban,, E., & Winslow,, R. L. (2006). A computational model integrating electrophysiology, contraction, and mitochondrial bioenergetics in the ventricular myocyte. Biophysical Journal, 91, 1564–1589.
Cortassa,, S., Aon,, M. A., Winslow,, R. L., & O`Rourke,, B. (2004). A mitochondrial oscillator dependent on reactive oxygen species. Biophysical Journal, 87, 2060–2073.
Dupont,, E., Matsushita,, T., Kaba,, R. A., Vozzi,, C., Coppen,, S. R., Khan,, N., … Severs,, N. J. (2001). Altered connexin expression in human congestive heart failure. Journal of Molecular and Cellular Cardiology, 33, 359–371.
Edwards,, A. G., Grandi,, E., Hake,, J. E., Patel,, S., Li,, P., Miyamoto,, S., … McCulloch,, A. D. (2014). Nonequilibrium reactivation of Na+ current drives early afterdepolarizations in mouse ventricle. Circulation. Arrhythmia and Electrophysiology, 7, 1205–1213.
Erickson,, J. R. (2014). Mechanisms of CaMKII activation in the heart. Frontiers in Pharmacology, 5, 59.
Erickson,, J. R., Joiner,, M. L., Guan,, X., Kutschke,, W., Yang,, J., Oddis,, C. V., … Anderson,, M. E. (2008). A dynamic pathway for calcium‐independent activation of CaMKII by methionine oxidation. Cell, 133, 462–474.
Erickson,, J. R., Nichols,, C. B., Uchinoumi,, H., Stein,, M. L., Bossuyt,, J., & Bers,, D. M. (2015). S‐Nitrosylation induces both autonomous activation and inhibition of calcium/calmodulin‐dependent protein kinase II delta. The Journal of Biological Chemistry, 290, 25646–25656.
Erickson,, J. R., Pereira,, L., Wang,, L., Han,, G., Ferguson,, A., Dao,, K., … Bers,, D. M. (2013). Diabetic hyperglycaemia activates CaMKII and arrhythmias by O‐linked glycosylation. Nature, 502, 372–376.
Fauconnier,, J., Lacampagne,, A., Rauzier,, J. M., Vassort,, G., & Richard,, S. (2005). Ca2+−dependent reduction of IK1 in rat ventricular cells: A novel paradigm for arrhythmia in heart failure? Cardiovascular Research, 68, 204–212.
Florea,, S. M., & Blatter,, L. A. (2010). The role of mitochondria for the regulation of cardiac alternans. Frontiers in Physiology, 1, 141.
Foteinou,, P. T., Greenstein,, J. L., & Winslow,, R. L. (2015). Mechanistic investigation of the arrhythmogenic role of oxidized CaMKII in the heart. Biophysical Journal, 109, 838–849.
Gaeta,, S. A., Bub,, G., Abbott,, G. W., & Christini,, D. J. (2009). Dynamical mechanism for subcellular alternans in cardiac myocytes. Circulation Research, 105, 335–342.
Gaeta,, S. A., Krogh‐Madsen,, T., & Christini,, D. J. (2010). Feedback‐control induced pattern formation in cardiac myocytes: A mathematical modeling study. Journal of Theoretical Biology, 266, 408–418.
Garny,, A., & Kohl,, P. (2004). Mechanical induction of arrhythmias during ventricular repolarization: Modeling cellular mechanisms and their interaction in two dimensions. Annals of the New York Academy of Sciences, 1015, 133–143.
Gauthier,, L. D., Greenstein,, J. L., Cortassa,, S., O`Rourke,, B., & Winslow,, R. L. (2013). A computational model of reactive oxygen species and redox balance in cardiac mitochondria. Biophysical Journal, 105, 1045–1056.
Gauthier,, L. D., Greenstein,, J. L., O`Rourke,, B., & Winslow,, R. L. (2013). An integrated mitochondrial ROS production and scavenging model: Implications for heart failure. Biophysical Journal, 105, 2832–2842.
Gintant,, G., Sager,, P. T., & Stockbridge,, N. (2016). Evolution of strategies to improve preclinical cardiac safety testing. Nature Reviews. Drug Discovery, 15, 457–471.
Glukhov,, A. V., Fedorov,, V. V., Lou,, Q., Ravikumar,, V. K., Kalish,, P. W., Schuessler,, R. B., … Efimov,, I. R. (2010). Transmural dispersion of repolarization in failing and nonfailing human ventricle. Circulation Research, 106, 981–991.
Gomez,, J. F., Cardona,, K., Martinez,, L., Saiz,, J., & Trenor,, B. (2014). Electrophysiological and structural remodeling in heart failure modulate arrhythmogenesis. 2D simulation study. PLoS One, 9, e103273.
Gomez,, J. F., Cardona,, K., Romero,, L., Ferrero,, J. M., Jr., & Trenor,, B. (2014). Electrophysiological and structural remodeling in heart failure modulate arrhythmogenesis. 1D simulation study. PLoS One, 9, e106602.
Grandi,, E., & Dobrev,, D. (2017). Non‐ion channel therapeutics for heart failure and atrial fibrillation: Are CaMKII inhibitors ready for clinical use? Journal of Molecular and Cellular Cardiology. In press. https://doi.org/10.1016/j.yjmcc.2017.10.010
Grandi,, E., & Herren,, A. W. (2014). CaMKII‐dependent regulation of cardiac Na+ homeostasis. Frontiers in Pharmacology, 5, 41.
Grandi,, E., Morotti,, S., Pueyo,, E., & Rodriguez,, B. (in press). Safety pharmacology—Risk assessment QT interval prolongation and beyond. Frontiers in Physiology, 9, 678.
Grandi,, E., Puglisi,, J. L., Wagner,, S., Maier,, L. S., Severi,, S., & Bers,, D. M. (2007). Simulation of Ca‐calmodulin‐dependent protein kinase II on rabbit ventricular myocyte ion currents and action potentials. Biophysical Journal, 93, 3835–3847.
Greenstein,, J. L., Hinch,, R., & Winslow,, R. L. (2006). Mechanisms of excitation‐contraction coupling in an integrative model of the cardiac ventricular myocyte. Biophysical Journal, 90, 77–91.
Guo,, T., Zhang,, T., Mestril,, R., & Bers,, D. M. (2006). Ca2+/calmodulin‐dependent protein kinase II phosphorylation of ryanodine receptor does affect calcium sparks in mouse ventricular myocytes. Circulation Research, 99, 398–406.
Hashambhoy,, Y. L., Greenstein,, J. L., & Winslow,, R. L. (2010). Role of CaMKII in RyR leak, EC coupling and action potential duration: A computational model. Journal of Molecular and Cellular Cardiology, 49, 617–624.
Hashambhoy,, Y. L., Winslow,, R. L., & Greenstein,, J. L. (2009). CaMKII‐induced shift in modal gating explains L‐type Ca2+ current facilitation: A modeling study. Biophysical Journal, 96, 1770–1785.
Hatano,, A., Okada,, J., Washio,, T., Hisada,, T., & Sugiura,, S. (2011). A three‐dimensional simulation model of cardiomyocyte integrating excitation‐contraction coupling and metabolism. Biophysical Journal, 101, 2601–2610.
Herren,, A. W., Bers,, D. M., & Grandi,, E. (2013). Post‐translational modifications of the cardiac Na channel: Contribution of CaMKII‐dependent phosphorylation to acquired arrhythmias. American Journal of Physiology. Heart and Circulatory Physiology, 305, H431–H445.
Hoch,, B., Meyer,, R., Hetzer,, R., Krause,, E. G., & Karczewski,, P. (1999). Identification and expression of delta‐isoforms of the multifunctional Ca2+/calmodulin‐dependent protein kinase in failing and nonfailing human myocardium. Circulation Research, 84, 713–721.
Hohendanner,, F., McCulloch,, A. D., Blatter,, L. A., & Michailova,, A. P. (2014). Calcium and IP3 dynamics in cardiac myocytes: Experimental and computational perspectives and approaches. Frontiers in Pharmacology, 5, 35.
Hu,, Y., Gurev,, V., Constantino,, J., Bayer,, J. D., & Trayanova,, N. A. (2013). Effects of mechano‐electric feedback on scroll wave stability in human ventricular fibrillation. PLoS One, 8, e60287.
Jacquemet,, V., & Henriquez,, C. S. (2007). Modelling cardiac fibroblasts: Interactions with myocytes and their impact on impulse propagation. Europace, 9(Suppl 6), vi29–vi37.
Jacquemet,, V., & Henriquez,, C. S. (2008). Loading effect of fibroblast‐myocyte coupling on resting potential, impulse propagation, and repolarization: Insights from a microstructure model. American Journal of Physiology. Heart and Circulatory Physiology, 294, H2040–H2052.
Jian,, Z., Han,, H., Zhang,, T., Puglisi,, J., Izu,, L. T., Shaw,, J. A., … Chen‐Izu,, Y. (2014). Mechanochemotransduction during cardiomyocyte contraction is mediated by localized nitric oxide signaling. Science Signaling, 7, ra27.
Johnstone,, R. H., Chang,, E. T., Bardenet,, R., de Boer,, T. P., Gavaghan,, D. J., Pathmanathan,, P., … Mirams,, G. R. (2016). Uncertainty and variability in models of the cardiac action potential: Can we build trustworthy models? Journal of Molecular and Cellular Cardiology, 96, 49–62.
Kang,, J. H., Lee,, H. S., Park,, D., Kang,, Y. W., Kim,, S. M., Gong,, J. R., & Cho,, K. H. (2017). Context‐independent essential regulatory interactions for apoptosis and hypertrophy in the cardiac signaling network. Scientific Reports, 7, 34.
Kembro,, J. M., Aon,, M. A., Winslow,, R. L., O`Rourke,, B., & Cortassa,, S. (2013). Integrating mitochondrial energetics, redox and ROS metabolic networks: A two‐compartment model. Biophysical Journal, 104, 332–343.
King,, J. H., Wickramarachchi,, C., Kua,, K., Du,, Y., Jeevaratnam,, K., Matthews,, H. R., … Fraser,, J. A. (2013). Loss of Nav1.5 expression and function in murine atria containing the RyR2‐P2328S gain‐of‐function mutation. Cardiovascular Research, 99, 751–759.
King,, J. H., Zhang,, Y., Lei,, M., Grace,, A. A., Huang,, C. L., & Fraser,, J. A. (2013). Atrial arrhythmia, triggering events and conduction abnormalities in isolated murine RyR2‐P2328S hearts. Acta Physiologica (Oxford, England), 207, 308–323.
Kirchhefer,, U., Schmitz,, W., Scholz,, H., & Neumann,, J. (1999). Activity of cAMP‐dependent protein kinase and Ca2+/calmodulin‐dependent protein kinase in failing and nonfailing human hearts. Cardiovascular Research, 42, 254–261.
Kohl,, P., & Camelliti,, P. (2007). Cardiac myocyte‐nonmyocyte electrotonic coupling: Implications for ventricular arrhythmogenesis. Heart Rhythm, 4, 233–235.
Kohlhaas,, M., Liu,, T., Knopp,, A., Zeller,, T., Ong,, M. F., Bohm,, M., … Maack,, C. (2010). Elevated cytosolic Na+ increases mitochondrial formation of reactive oxygen species in failing cardiac myocytes. Circulation, 121, 1606–1613.
Kreusser,, M. M., & Backs,, J. (2014). Integrated mechanisms of CaMKII‐dependent ventricular remodeling. Frontiers in Pharmacology, 5, 36.
Krogh‐Madsen,, T., & Christini,, D. J. (2007). Action potential duration dispersion and alternans in simulated heterogeneous cardiac tissue with a structural barrier. Biophysical Journal, 92, 1138–1149.
Krogh‐Madsen,, T., & Christini,, D. J. (2017). Slow [Na+]i dynamics impacts arrhythmogenesis and spiral wave reentry in cardiac myocyte ionic model. Chaos, 27, 093907.
Lang,, D., Sato,, D., Jiang,, Y., Ginsburg,, K. S., Ripplinger,, C. M., & Bers,, D. M. (2017). Calcium‐dependent Arrhythmogenic foci created by weakly coupled Myocytes in the failing heart. Circulation Research, 121, 1379–1391.
Li,, L., Satoh,, H., Ginsburg,, K. S., & Bers,, D. M. (1997). The effect of Ca2+‐calmodulin‐dependent protein kinase II on cardiac excitation‐contraction coupling in ferret ventricular myocytes. The Journal of Physiology, 501(Pt 1), 17–31.
Li,, Q., Su,, D., O`Rourke,, B., Pogwizd,, S. M., & Zhou,, L. (2015). Mitochondria‐derived ROS bursts disturb Ca2+ cycling and induce abnormal automaticity in Guinea pig cardiomyocytes: A theoretical study. American Journal of Physiology. Heart and Circulatory Physiology, 308, H623–H636.
Li,, W., Kohl,, P., & Trayanova,, N. (2004). Induction of ventricular arrhythmias following mechanical impact: A simulation study in 3D. Journal of Molecular Histology, 35, 679–686.
Li,, W., Kohl,, P., & Trayanova,, N. (2006). Myocardial ischemia lowers precordial thump efficacy: An inquiry into mechanisms using three‐dimensional simulations. Heart Rhythm, 3, 179–186.
Limbu,, S., Hoang‐Trong,, T. M., Prosser,, B. L., Lederer,, W. J., & Jafri,, M. S. (2015). Modeling local X‐ROS and calcium signaling in the heart. Biophysical Journal, 109, 2037–2050.
Ling,, H., Zhang,, T., Pereira,, L., Means,, C. K., Cheng,, H., Gu,, Y., … Brown,, J. H. (2009). Requirement for Ca2+/calmodulin‐dependent kinase II in the transition from pressure overload‐induced cardiac hypertrophy to heart failure in mice. The Journal of Clinical Investigation, 119, 1230–1240.
Lou,, Q., Fedorov,, V. V., Glukhov,, A. V., Moazami,, N., Fast,, V. G., & Efimov,, I. R. (2011). Transmural heterogeneity and remodeling of ventricular excitation‐contraction coupling in human heart failure. Circulation, 123, 1881–1890.
Louch,, W. E., Hake,, J., Mork,, H. K., Hougen,, K., Skrbic,, B., Ursu,, D., … Sejersted,, O. M. (2013). Slow Ca2+ sparks de‐synchronize Ca2+ release in failing cardiomyocytes: Evidence for altered configuration of Ca2+ release units? Journal of Molecular and Cellular Cardiology, 58, 41–52.
Maack,, C., Cortassa,, S., Aon,, M. A., Ganesan,, A. N., Liu,, T., & O`Rourke,, B. (2006). Elevated cytosolic Na+ decreases mitochondrial Ca2+ uptake during excitation‐contraction coupling and impairs energetic adaptation in cardiac myocytes. Circulation Research, 99, 172–182.
MacCannell,, K. A., Bazzazi,, H., Chilton,, L., Shibukawa,, Y., Clark,, R. B., & Giles,, W. R. (2007). A mathematical model of electrotonic interactions between ventricular myocytes and fibroblasts. Biophysical Journal, 92, 4121–4132.
Maier,, L. S., & Bers,, D. M. (2007). Role of Ca2+/calmodulin‐dependent protein kinase (CaMK) in excitation‐contraction coupling in the heart. Cardiovascular Research, 73, 631–640.
McDowell,, K. S., Arevalo,, H. J., Maleckar,, M. M., & Trayanova,, N. A. (2011). Susceptibility to arrhythmia in the infarcted heart depends on myofibroblast density. Biophysical Journal, 101, 1307–1315.
Michailova,, A., & Spassov,, V. (1997). Computer simulation of excitation‐contraction coupling in cardiac muscle. A study of the regulatory role of calcium binding to troponin C. General Physiology and Biophysics, 16, 29–38.
Michailova,, A. P., & Spassov,, V. Z. (1992). Theoretical model and computer simulation of excitation‐contraction coupling of mammalian cardiac muscle. Journal of Molecular and Cellular Cardiology, 24, 97–104.
Mirams,, G. R., Pathmanathan,, P., Gray,, R. A., Challenor,, P., & Clayton,, R. H. (2016). Uncertainty and variability in computational and mathematical models of cardiac physiology. The Journal of Physiology, 594, 6833–6847.
Molkentin,, J. D. (2004). Calcineurin‐NFAT signaling regulates the cardiac hypertrophic response in coordination with the MAPKs. Cardiovascular Research, 63, 467–475.
Moreno,, J. D., Yang,, P. C., Bankston,, J. R., Grandi,, E., Bers,, D. M., Kass,, R. S., & Clancy,, C. E. (2013). Ranolazine for congenital and acquired late INa linked arrhythmias: In silico pharmacologic screening. Circulation Research, 113, e50–e61.
Morotti,, S., Edwards,, A. G., McCulloch,, A. D., Bers,, D. M., & Grandi,, E. (2014). A novel computational model of mouse myocyte electrophysiology to assess the synergy between Na+ loading and CaMKII. The Journal of Physiology, 592, 1181–1197.
Morotti,, S., & Grandi,, E. (2017). Logistic regression analysis of populations of electrophysiological models to assess proarrythmic risk. MethodsX, 4, 25–34.
Morotti,, S., McCulloch,, A. D., Bers,, D. M., Edwards,, A. G., & Grandi,, E. (2016). Atrial‐selective targeting of arrhythmogenic phase‐3 early afterdepolarizations in human myocytes. Journal of Molecular and Cellular Cardiology, 96, 63–71.
Myles,, R. C., Wang,, L., Kang,, C., Bers,, D. M., & Ripplinger,, C. M. (2012). Local beta‐adrenergic stimulation overcomes source‐sink mismatch to generate focal arrhythmia. Circulation Research, 110, 1454–1464.
Nayak,, A. R., Shajahan,, T. K., Panfilov,, A. V., & Pandit,, R. (2013). Spiral‐wave dynamics in a mathematical model of human ventricular tissue with myocytes and fibroblasts. PLoS One, 8, e72950.
Negroni,, J. A., Morotti,, S., Lascano,, E. C., Gomes,, A. V., Grandi,, E., Puglisi,, J. L., & Bers,, D. M. (2015). Beta‐adrenergic effects on cardiac myofilaments and contraction in an integrated rabbit ventricular myocyte model. Journal of Molecular and Cellular Cardiology, 81, 162–175.
Niederer,, S. A., & Smith,, N. P. (2007). A mathematical model of the slow force response to stretch in rat ventricular myocytes. Biophysical Journal, 92, 4030–4044.
Nivala,, M., Korge,, P., Nivala,, M., Weiss,, J. N., & Qu,, Z. (2011). Linking flickering to waves and whole‐cell oscillations in a mitochondrial network model. Biophysical Journal, 101, 2102–2111.
Nivala,, M., Song,, Z., Weiss,, J. N., & Qu,, Z. (2015). T‐tubule disruption promotes calcium alternans in failing ventricular myocytes: Mechanistic insights from computational modeling. Journal of Molecular and Cellular Cardiology, 79, 32–41.
Onal,, B., Gratz,, D., & Hund,, T. J. (2017). Ca2+/calmodulin kinase II‐dependent regulation of atrial myocyte late Na+ current, Ca2+ cycling and excitability: A mathematical modeling study. American Journal of Physiology‐Heart and Circulatory Physiology, 313(6), H1227–H1239.
Oyehaug,, L., Loose,, K. O., Jolle,, G. F., Roe,, A. T., Sjaastad,, I., Christensen,, G., … Louch,, W. E. (2013). Synchrony of cardiomyocyte Ca2+ release is controlled by T‐tubule organization, SR Ca2+ content, and ryanodine receptor Ca2+ sensitivity. Biophysical Journal, 104, 1685–1697.
Pereira,, L., Bare,, D. J., Galice,, S., Shannon,, T. R., & Bers,, D. M. (2017). Beta‐adrenergic induced SR Ca2+ leak is mediated by an Epac‐NOS pathway. Journal of Molecular and Cellular Cardiology, 108, 8–16.
Peyronnet,, R., Nerbonne,, J. M., & Kohl,, P. (2016). Cardiac mechano‐gated ion channels and arrhythmias. Circulation Research, 118, 311–329.
Poelzing,, S., & Rosenbaum,, D. S. (2004). Altered connexin43 expression produces arrhythmia substrate in heart failure. American Journal of Physiology. Heart and Circulatory Physiology, 287, H1762–H1770.
Pogwizd,, S. M., Schlotthauer,, K., Li,, L., Yuan,, W., & Bers,, D. M. (2001). Arrhythmogenesis and contractile dysfunction in heart failure: Roles of sodium‐calcium exchange, inward rectifier potassium current, and residual beta‐adrenergic responsiveness. Circulation Research, 88, 1159–1167.
Prosser,, B. L., Ward,, C. W., & Lederer,, W. J. (2011). X‐ROS signaling: Rapid mechano‐chemo transduction in heart. Science, 333, 1440–1445.
Prosser,, B. L., Ward,, C. W., & Lederer,, W. J. (2013). X‐ROS signalling is enhanced and graded by cyclic cardiomyocyte stretch. Cardiovascular Research, 98, 307–314.
Qu,, Z., Karagueuzian,, H. S., Garfinkel,, A., & Weiss,, J. N. (2004). Effects of Na+ channel and cell coupling abnormalities on vulnerability to reentry: A simulation study. American Journal of Physiology. Heart and Circulatory Physiology, 286, H1310–H1321.
Rice,, J. J., Wang,, F., Bers,, D. M., & de Tombe,, P. P. (2008). Approximate model of cooperative activation and crossbridge cycling in cardiac muscle using ordinary differential equations. Biophysical Journal, 95, 2368–2390.
Ripplinger,, C. M., Noujaim,, S. F., & Linz,, D. (2016). The nervous heart. Progress in Biophysics and Molecular Biology, 120, 199–209.
Ryall,, K. A., Bezzerides,, V. J., Rosenzweig,, A., & Saucerman,, J. J. (2014). Phenotypic screen quantifying differential regulation of cardiac myocyte hypertrophy identifies CITED4 regulation of myocyte elongation. Journal of Molecular and Cellular Cardiology, 72, 74–84.
Ryall,, K. A., Holland,, D. O., Delaney,, K. A., Kraeutler,, M. J., Parker,, A. J., & Saucerman,, J. J. (2012). Network reconstruction and systems analysis of cardiac myocyte hypertrophy signaling. The Journal of Biological Chemistry, 287, 42259–42268.
Sachse,, F. B., Moreno,, A. P., & Abildskov,, J. A. (2008). Electrophysiological modeling of fibroblasts and their interaction with myocytes. Annals of Biomedical Engineering, 36, 41–56.
Sachse,, F. B., Moreno,, A. P., Seemann,, G., & Abildskov,, J. A. (2009). A model of electrical conduction in cardiac tissue including fibroblasts. Annals of Biomedical Engineering, 37, 874–889.
Sarkar,, A. X., Christini,, D. J., & Sobie,, E. A. (2012). Exploiting mathematical models to illuminate electrophysiological variability between individuals. The Journal of Physiology, 590, 2555–2567.
Sato,, T., Ohkusa,, T., Honjo,, H., Suzuki,, S., Yoshida,, M. A., Ishiguro,, Y. S., … Matsuzaki,, M. (2008). Altered expression of connexin43 contributes to the arrhythmogenic substrate during the development of heart failure in cardiomyopathic hamster. American Journal of Physiology. Heart and Circulatory Physiology, 294, H1164–H1173.
Shannon,, T. R., Wang,, F., & Bers,, D. M. (2005). Regulation of cardiac sarcoplasmic reticulum Ca release by luminal [Ca] and altered gating assessed with a mathematical model. Biophysical Journal, 89, 4096–4110.
Shiferaw,, Y., & Karma,, A. (2006). Turing instability mediated by voltage and calcium diffusion in paced cardiac cells. Proceedings of the National Academy of Sciences of the United States of America, 103, 5670–5675.
Sobie,, E. A. (2009). Parameter sensitivity analysis in electrophysiological models using multivariable regression. Biophysical Journal, 96, 1264–1274.
Soltis,, A. R., & Saucerman,, J. J. (2010). Synergy between CaMKII substrates and beta‐adrenergic signaling in regulation of cardiac myocyte Ca2+ handling. Biophysical Journal, 99, 2038–2047.
Sridhar,, S., Vandersickel,, N., & Panfilov,, A. V. (2017). Effect of myocyte‐fibroblast coupling on the onset of pathological dynamics in a model of ventricular tissue. Scientific Reports, 7, 40985.
Surdo,, N. C., Berrera,, M., Koschinski,, A., Brescia,, M., Machado,, M. R., Carr,, C., … Zaccolo,, M. (2017). FRET biosensor uncovers cAMP nano‐domains at beta‐adrenergic targets that dictate precise tuning of cardiac contractility. Nature Communications, 8, 15031.
Takanari,, H., Bourgonje,, V. J., Fontes,, M. S., Raaijmakers,, A. J., Driessen,, H., Jansen,, J. A., … Vos,, M. A. (2016). Calmodulin/CaMKII inhibition improves intercellular communication and impulse propagation in the heart and is antiarrhythmic under conditions when fibrosis is absent. Cardiovascular Research, 111, 410–421.
Tan,, P. M., Buchholz,, K. S., Omens,, J. H., McCulloch,, A. D., & Saucerman,, J. J. (2017). Predictive model identifies key network regulators of cardiomyocyte mechano‐signaling. PLoS Computational Biology, 13, e1005854.
Tewari,, S. G., Bugenhagen,, S. M., Vinnakota,, K. C., Rice,, J. J., Janssen,, P. M. L., & Beard,, D. A. (2016). Influence of metabolic dysfunction on cardiac mechanics in decompensated hypertrophy and heart failure. Journal of Molecular and Cellular Cardiology, 94, 162–175.
Timmermann,, V., Dejgaard,, L. A., Haugaa,, K. H., Edwards,, A. G., Sundnes,, J., McCulloch,, A. D., & Wall,, S. T. (2017). An integrative appraisal of mechano‐electric feedback mechanisms in the heart. Progress in Biophysics and Molecular Biology, 130, 404–417.
Wagner,, S., Dybkova,, N., Rasenack,, E. C., Jacobshagen,, C., Fabritz,, L., Kirchhof,, P., … Maier,, L. S. (2006). Ca2+/calmodulin‐dependent protein kinase II regulates cardiac Na+ channels. The Journal of Clinical Investigation, 116, 3127–3138.
Wagner,, S., Ruff,, H. M., Weber,, S. L., Bellmann,, S., Sowa,, T., Schulte,, T., … Maier,, L. S. (2011). Reactive oxygen species‐activated Ca/calmodulin kinase IIdelta is required for late I(Na) augmentation leading to cellular Na and Ca overload. Circulation Research, 108, 555–565.
Wei,, A. C., Aon,, M. A., O`Rourke,, B., Winslow,, R. L., & Cortassa,, S. (2011). Mitochondrial energetics, pH regulation, and ion dynamics: A computational‐experimental approach. Biophysical Journal, 100, 2894–2903.
Weiss,, J. N., Garfinkel,, A., Karagueuzian,, H. S., Chen,, P. S., & Qu,, Z. (2010). Early afterdepolarizations and cardiac arrhythmias. Heart Rhythm, 7, 1891–1899.
Wilson,, L. D., Jeyaraj,, D., Wan,, X., Hoeker,, G. S., Said,, T. H., Gittinger,, M., … Rosenbaum,, D. S. (2009). Heart failure enhances susceptibility to arrhythmogenic cardiac alternans. Heart Rhythm, 6, 251–259.
Xie,, F., Qu,, Z., Garfinkel,, A., & Weiss,, J. N. (2001). Electrophysiological heterogeneity and stability of reentry in simulated cardiac tissue. American Journal of Physiology. Heart and Circulatory Physiology, 280, H535–H545.
Xie,, L. H., Chen,, F., Karagueuzian,, H. S., & Weiss,, J. N. (2009). Oxidative‐stress‐induced afterdepolarizations and calmodulin kinase II signaling. Circulation Research, 104, 79–86.
Xie,, L. H., & Weiss,, J. N. (2009). Arrhythmogenic consequences of intracellular calcium waves. American Journal of Physiology. Heart and Circulatory Physiology, 297, H997–H1002.
Xie,, Y., Garfinkel,, A., Camelliti,, P., Kohl,, P., Weiss,, J. N., & Qu,, Z. (2009). Effects of fibroblast‐myocyte coupling on cardiac conduction and vulnerability to reentry: A computational study. Heart Rhythm, 6, 1641–1649.
Xie,, Y., Garfinkel,, A., Weiss,, J. N., & Qu,, Z. (2009). Cardiac alternans induced by fibroblast‐myocyte coupling: Mechanistic insights from computational models. American Journal of Physiology. Heart and Circulatory Physiology, 297, H775–H784.
Xie,, Y., Liao,, Z., Grandi,, E., Shiferaw,, Y., & Bers,, D. M. (2015). Slow [Na]i changes and positive feedback between membrane potential and [Ca]i underlie intermittent early Afterdepolarizations and arrhythmias. Circulation. Arrhythmia and Electrophysiology, 8, 1472–1480.
Xie,, Y., Sato,, D., Garfinkel,, A., Qu,, Z., & Weiss,, J. N. (2010). So little source, so much sink: Requirements for afterdepolarizations to propagate in tissue. Biophysical Journal, 99, 1408–1415.
Yang,, L., Korge,, P., Weiss,, J. N., & Qu,, Z. (2010). Mitochondrial oscillations and waves in cardiac myocytes: Insights from computational models. Biophysical Journal, 98, 1428–1438.
Yaniv,, Y., Stanley,, W. C., Saidel,, G. M., Cabrera,, M. E., & Landesberg,, A. (2008). The role of Ca2+ in coupling cardiac metabolism with regulation of contraction: In silico modeling. Annals of the New York Academy of Sciences, 1123, 69–78.
Yao,, L., Fan,, P., Jiang,, Z., Viatchenko‐Karpinski,, S., Wu,, Y., Kornyeyev,, D., … Belardinelli,, L. (2011). Nav1.5‐dependent persistent Na+ influx activates CaMKII in rat ventricular myocytes and N1325S mice. American Journal of Physiology. Cell Physiology, 301, C577–C586.
Zahid,, S., Whyte,, K. N., Schwarz,, E. L., Blake,, R. C., 3rd, Boyle,, P. M., Chrispin,, J., … Trayanova,, N. A. (2016). Feasibility of using patient‐specific models and the "minimum cut" algorithm to predict optimal ablation targets for left atrial flutter. Heart Rhythm, 13, 1687–1698.
Zeigler,, A. C., Richardson,, W. J., Holmes,, J. W., & Saucerman,, J. J. (2016). A computational model of cardiac fibroblast signaling predicts context‐dependent drivers of myofibroblast differentiation. Journal of Molecular and Cellular Cardiology, 94, 72–81.
Zhang,, T., Johnson,, E. N., Gu,, Y., Morissette,, M. R., Sah,, V. P., Gigena,, M. S., … Brown,, J. H. (2002). The cardiac‐specific nuclear delta(B) isoform of Ca2+/calmodulin‐dependent protein kinase II induces hypertrophy and dilated cardiomyopathy associated with increased protein phosphatase 2A activity. The Journal of Biological Chemistry, 277, 1261–1267.
Zhang,, T., Maier,, L. S., Dalton,, N. D., Miyamoto,, S., Ross,, J., Jr., Bers,, D. M., & Brown,, J. H. (2003). The deltaC isoform of CaMKII is activated in cardiac hypertrophy and induces dilated cardiomyopathy and heart failure. Circulation Research, 92, 912–919.
Zhou,, L., Cortassa,, S., Wei,, A. C., Aon,, M. A., Winslow,, R. L., & O`Rourke,, B. (2009). Modeling cardiac action potential shortening driven by oxidative stress‐induced mitochondrial oscillations in Guinea pig cardiomyocytes. Biophysical Journal, 97, 1843–1852.
Zhou,, L., Solhjoo,, S., Millare,, B., Plank,, G., Abraham,, M. R., Cortassa,, S., … O`Rourke,, B. (2014). Effects of regional mitochondrial depolarization on electrical propagation: Implications for arrhythmogenesis. Circulation. Arrhythmia and Electrophysiology, 7, 143–151.
Zile,, M. A., & Trayanova,, N. A. (2016). Rate‐dependent force, intracellular calcium, and action potential voltage alternans are modulated by sarcomere length and heart failure induced‐remodeling of thin filament regulation in human heart failure: A myocyte modeling study. Progress in Biophysics and Molecular Biology, 120, 270–280.
Zile,, M. A., & Trayanova,, N. A. (2017). Myofilament protein dynamics modulate EAD formation in human hypertrophic cardiomyopathy. Progress in Biophysics and Molecular Biology, 130, 418–428.