Research Topics
| M E AndersonSummaryAffiliation: Vanderbilt University Country: USA Publications
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Publications
Calmodulin kinase signaling in heart: an intriguing candidate target for therapy of myocardial dysfunction and arrhythmiasMark E Anderson
Vanderbilt University Medical Center, 383 Preston Research Building, Nashville, TN 37232 6300, USA
Pharmacol Ther 106:39-55. 2005..This review discusses CaMKII structure and function and recent evidence implicating CaMKII inhibition as a potential strategy for treating myocardial dysfunction and arrhythmias in the setting of structural heart disease...- QT interval prolongation and arrhythmia: an unbreakable connection?M E Anderson
Department of Cardiovascular Medicine, Vanderbilt University Medical School, Nashville, TN, USA
J Intern Med 259:81-90. 2006..CaMKII is one of these molecules and CaMKII activity is at least partially responsible for the proarrhythmic consequences of excessive QT interval prolongation... - Calmodulin kinase and L-type calcium channels; a recipe for arrhythmias?Mark E Anderson
Division of Cardiovascular Medicine, Departments of Medicine and Pharmacology, Vanderbilt University Medical Center, 383 Preston Research Building, 2220 Pierce Avenue, Nashville, TN 37232 6300, USA
Trends Cardiovasc Med 14:152-61. 2004..LTCC dysregulation is discussed in the context of new results showing that CaMKII can be a proarrhythmic signal in disease conditions in which Ca2+(i) is disordered and cardiac repolarization is excessively prolonged... - Calmodulin kinase is a molecular switch for cardiac excitation-contraction couplingY Wu
Department of Internal Medicine, Vanderbilt University, Nashville, TN 37232, USA
Proc Natl Acad Sci U S A 98:2877-81. 2001..These findings support the hypothesis that CaMK is required to functionally couple LTCC and RyR during cardiac ECC... - Calmodulin inhibitor W-7 unmasks a novel electrocardiographic parameter that predicts initiation of torsade de pointesT David Gbadebo
Department of Medicine, Vanderbilt University Medical Center, Nashville, Tenn 37232-6300, USA
Circulation 105:770-4. 2002.... - Calmodulin kinase II and arrhythmias in a mouse model of cardiac hypertrophyYuejin Wu
Department of Internal Medicine, Vanderbilt University, Nashville, Tenn, USA
Circulation 106:1288-93. 2002..Cellular studies point to EADs as a triggering mechanism for arrhythmias but suggest that the increase in arrhythmias after beta-adrenergic stimulation is independent of enhanced EAD frequency... - Calmodulin and the philosopher's stone: Changing Ca2+ into arrhythmiasMark E Anderson
Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee 37232 6300, USA
J Cardiovasc Electrophysiol 13:195-7. 2002..This article will examine the implications of these recent findings for arrhythmogenesis and the development of new antiarrhythmic therapies... - Cardiac ion channelsDan M Roden
Departments of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA
Annu Rev Physiol 64:431-75. 2002..This review discusses these new tools and how their application to the problem of arrhythmias is generating new mechanistic insights to identify patients at risk for this condition and developing improved antiarrhythmic therapies... - Cardiac repolarization: current knowledge, critical gaps, and new approaches to drug development and patient managementMark E Anderson
Vanderbilt University Medical Center, Nashville, Tenn 37232-6300, USA
Am Heart J 144:769-81. 2002 - Frequency of late recurrence of intra-atrial reentry tachycardia after radiofrequency catheter ablation in patients with congenital heart diseasePrince J Kannankeril
Department of Medicine, Vanderbilty University Medical Center, Nashville, Tennessee 37232 2572, USA
Am J Cardiol 92:879-81. 2003..Of the 23 patients who were free of recurrence 1 year after ablation, 21 (91%) remain free from recurrence at an average of 45 months (median 39; range 15 to 88) after ablation... - Temporal changes in ventricular function assessed echocardiographically in conscious and anesthetized miceJeffrey N Rottman
Department of Internal Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232 6300, USA
J Am Soc Echocardiogr 16:1150-7. 2003..Serial echocardiographic assessments of cardiac function, dimension, and mass can be performed with high reproducibility in conscious mice... - Potassium current antagonist properties and proarrhythmic consequences of quinolone antibioticsM E Anderson
Vanderbilt University Medical Center, Department of Internal Medicine and Pharmacology, Divisions of Clinical Pharmacology and Cardiovascular Medicine, Nashville, Tennessee 37232 6300, USA
J Pharmacol Exp Ther 296:806-10. 2001..These findings show that I(Kr) block may be a common feature of many quinolone antibiotics, and that the proarrhythmic consequences vary according to I(Kr) antagonist potency, but are also influenced by additional, unidentified factors... - Replacement by homologous recombination of the minK gene with lacZ reveals restriction of minK expression to the mouse cardiac conduction systemS Kupershmidt
Departments of Medicine Pharmacology, Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, TN, USA
Circ Res 84:146-52. 1999..More generally, the restricted nature of minK expression in the mouse heart suggests species-specific roles of this gene product in mediating the electrophysiological properties of the heart... - A ?(IV)-spectrin/CaMKII signaling complex is essential for membrane excitability in miceThomas J Hund
Department of Internal Medicine, Division of Cardiovascular Medicine, University of Iowa Carver College of Medicine, Iowa City, Iowa 52242, USA
J Clin Invest 120:3508-19. 2010..Collectively, our data define an unexpected but indispensable molecular platform that determines membrane excitability in the mouse heart and brain... - Reduced repolarization reserve in ventricular myocytes from female miceYuejin Wu
Department of Medicine, 315 Preston Research Building II, Vanderbilt University Medical Center, Nashville, TN 37232-6300, USA
Cardiovasc Res 53:763-9. 2002..Female mice have reduced RR that is unmasked by FK506. These findings suggest that gender is an important variable for cardiovascular studies using mice... - Proarrhythmic defects in Timothy syndrome require calmodulin kinase IIWilliam H Thiel
Vanderbilt University, Nashville, TN, USA
Circulation 118:2225-34. 2008..2 current (I(Ca)). During cellular Ca(2+) overload, the calmodulin-dependent protein kinase II (CaMKII) causes arrhythmias. We hypothesized that CaMKII is a part of the proarrhythmic mechanism in TS... - Calmodulin kinase is functionally targeted to the action potential plateau for regulation of L-type Ca2+ current in rabbit cardiomyocytesYuejin Wu
Department of Internal Medicine, Vanderbilt University Medical Center, Nashville, TN 37232-6300, USA
J Physiol 554:145-55. 2004..These findings show that ICa-L responses to CaMK are voltage dependent and suggest a new model of L-type Ca2+ channel regulation where voltage-dependent changes control ICa-L responses to Ca2+-CaM and CaMK signalling... - Calmodulin kinase and a calmodulin-binding 'IQ' domain facilitate L-type Ca2+ current in rabbit ventricular myocytes by a common mechanismY Wu
Department of Internal Medicine, Vanderbilt University, Nashville, TN 37232-6300, USA
J Physiol 535:679-87. 2001..Both CaMK and IQmp were able to induce a modal gating shift in LTCCs, suggesting that each of these signalling elements is important for Ca2+-CaM-dependent LTCC facilitation in cardiac myocytes... - Ca2+-dependent regulation of cardiac L-type Ca2+ channels: is a unifying mechanism at hand?M E Anderson
Department of Internal Medicine, Vanderbilt University, Nashville, Tennessee 37232, USA
J Mol Cell Cardiol 33:639-50. 2001..A recent explosion of work has shed new light on the mechanisms and molecular identity of domains necessary for [Ca2+]i-dependent regulation of LTCC... - Calmodulin kinase II inhibition protects against structural heart diseaseRong Zhang
Department of Medicine, Vanderbilt University School of Medicine, 2220 Pierce Avenue, Nashville, Tennessee 37232 6300, USA
Nat Med 11:409-17. 2005..These findings mark CaMKII as a determinant of clinically important heart disease phenotypes, and suggest CaMKII inhibition can be a highly selective approach for targeting adverse myocardial remodeling linked to betaAR signaling... - Atrial fibrillation in KCNE1-null miceJoel Temple
Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tenn 37232 6602, USA
Circ Res 97:62-9. 2005..Thus, KCNE1 deletion in mice unexpectedly leads to increased outward current in atrial myocytes, shortens atrial action potentials, and enhances susceptibility to atrial fibrillation... - An EF-hand in the sodium channel couples intracellular calcium to cardiac excitabilityTammy L Wingo
Department of Pharmacology, Vanderbilt University, Nashville, Tennessee 37232, USA
Nat Struct Mol Biol 11:219-25. 2004..These studies reveal the molecular basis for certain forms of long QT syndrome and other arrhythmia-producing syndromes, and suggest a potential pharmacological target for antiarrhythmic drug design... - Death, cardiac dysfunction, and arrhythmias are increased by calmodulin kinase II in calcineurin cardiomyopathyMichelle S C Khoo
Department of Medicine, Vanderbilt University, Nashville, Tenn, USA
Circulation 114:1352-9. 2006.... - C terminus L-type Ca2+ channel calmodulin-binding domains are 'auto-agonist' ligands in rabbit ventricular myocytesIgor Dzhura
Department of Internal Medicine, Vanderbilt University, Nashville, TN 37232, USA
J Physiol 550:731-8. 2003..CBmp and CaMKII increased L-type Ca2+ channel Po in a non-additive manner, suggesting that low and high Ca(2+)-CaM-dependent L-type Ca2+ channel facilitation pathways converge upon a common signalling mechanism... - CaMKII, an emerging molecular driver for calcium homeostasis, arrhythmias, and cardiac dysfunctionChad E Grueter
Department of Molecular Physiology and Biophysics, Vanderbilt University Medical Center, Nashville, TN, USA
J Mol Med (Berl) 85:5-14. 2007..Moreover, CaMKII was recently identified as a potential drug target in cardiac disease. This work has given us a closer view of the complexity and therapeutic possibilities of CaMKII regulation of Ca(2+) signaling in cardiac myocytes... - A dynamic alpha-beta inter-subunit agonist signaling complex is a novel feedback mechanism for regulating L-type Ca2+ channel openingRong Zhang
Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA
FASEB J 19:1573-5. 2005..Thus, the bifunctional ability of the alpha subunit CaM binding motifs to competitively associate with the beta subunit or CaM provides a novel paradigm for feedback control of cellular Ca2+ entry... - Mice with the R176Q cardiac ryanodine receptor mutation exhibit catecholamine-induced ventricular tachycardia and cardiomyopathyPrince J Kannankeril
Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, TN 37232, USA
Proc Natl Acad Sci U S A 103:12179-84. 2006..Our results suggest that the R176Q mutation in RyR2 predisposes the heart to catecholamine-induced oscillatory calcium-release events that trigger a calcium-dependent ventricular arrhythmia... - Calmodulin kinase II inhibition protects against myocardial cell apoptosis in vivoYingbo Yang
Dept of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA
Am J Physiol Heart Circ Physiol 291:H3065-75. 2006..These findings indicate CaMKII is proapoptotic in vivo and suggest that regulation of SR Ca(2+) content by PLN contributes to the antiapoptotic mechanism of CaMKII inhibition... - Local control of Ca2+-induced Ca2+ release in mouse sinoatrial node cellsBiyi Chen
Division of Cardiovascular Medicine, Department of Internal Medicine, University of Iowa Carver College of Medicine, 285 Newton Road, Iowa City, IA 52242, USA
J Mol Cell Cardiol 47:706-15. 2009..We concluded that the "local control" mechanism of CICR is responsible for both local Ca2+ release during diastolic depolarization and the synchronized Ca2+ transients observed during action potential in SAN cells... - Oxidative mediated lipid peroxidation recapitulates proarrhythmic effects on cardiac sodium channelsKoji Fukuda
Department of Anesthesiology, Vanderbilt University School of Medicine, Nashville, TN, USA
Circ Res 97:1262-9. 2005..These data suggest Na+ channel dysfunction evoked by lipid peroxidation is a candidate mechanism for ischemia-related conduction abnormalities and arrhythmias... - Polymorphic ventricular tachycardia and abnormal Ca2+ handling in very-long-chain acyl-CoA dehydrogenase null miceAndreas A Werdich
Division of Cardiology, Department of Pediatrics, Vanderbilt University School of Medicine, Nashville, TN 37232 0001, USA
Am J Physiol Heart Circ Physiol 292:H2202-11. 2007..We conclude that intracellular Ca(2+) handling represents a possible molecular mechanism of arrhythmias in mice and perhaps in VLCAD-deficient humans... - Cytoskeletal disrupting agents prevent calmodulin kinase, IQ domain and voltage-dependent facilitation of L-type Ca2+ channelsIgor Dzhura
Department of Internal Medicine, Vanderbilt University Medical Center, Vanderbilt University, Nashville, TN 37232-6300, USA
J Physiol 545:399-406. 2002.... - Pause-dependent polymorphic ventricular tachycardia during long-term treatment with dofetilide: a placebo-controlled, implantable cardioverter-defibrillator-based evaluationA Mazur
Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA
J Am Coll Cardiol 37:1100-5. 2001..These data suggest that in ICD patients either long-term dofetilide therapy is associated with an increased risk of TdP or the drug alters VT morphology... - Functional similarity between electrograms recorded from an implantable cardioverter defibrillator emulator and the surface electrocardiogramA Mazur
Vanderbilt University Medical Center, Nashville, Tennessee 37232-6300, USA
Pacing Clin Electrophysiol 24:34-40. 2001..They also may be useful as a surrogate of the ECG for analysis and monitoring of different components of P-QRS-T complex... - L-type Ca2+ channel facilitation mediated by phosphorylation of the beta subunit by CaMKIIChad E Grueter
Department of Molecular Physiology and Biophysics, Vanderbilt University Medical Center, Nashville, Tennessee 37232, USA
Mol Cell 23:641-50. 2006..These findings reveal a molecular mechanism for targeting CaMKII to LTCCs and facilitating I(Ca) that may modulate Ca(2+) entry in diverse cell types coexpressing CaMKII and the beta(2a) subunit... - The role of calmodulin kinase II in myocardial physiology and diseaseLuis F Couchonnal
Departments of Internal Medicine, Division of Cardiovascular Medicine, University of Iowa, Carver College of Medicine, Iowa City, Iowa, USA
Physiology (Bethesda) 23:151-9. 2008..Under stress conditions, excessive CaMKII activity promotes heart failure and arrhythmias, in part through actions at Ca(2+) homeostatic proteins. Here, we briefly review the molecular and cellular physiology of CaMKII in myocardium... - Ca2+/calmodulin-dependent kinase II triggers cell membrane injury by inducing complement factor B gene expression in the mouse heartMadhu V Singh
Division of Cardiovascular Medicine, Carver College of Medicine, University of Iowa, Iowa City, Iowa 52242, USA
J Clin Invest 119:986-96. 2009..Our findings demonstrate what we believe is a novel target for CaMKII in myocardial injury and suggest that CaMKII is broadly important for the genetic effects of MI in cardiomyocytes... - Ankyrin-B regulates Kir6.2 membrane expression and function in heartJingdong Li
Division of Cardiovascular Medicine, Department of Internal Medicine, University of Iowa Carver College of Medicine, Iowa City, Iowa 52242, USA
J Biol Chem 285:28723-30. 2010..Collectively, our new findings define a new role for cardiac ankyrin polypeptides in regulation of ion channel membrane expression in heart... - Differential regulated interactions of calcium/calmodulin-dependent protein kinase II with isoforms of voltage-gated calcium channel beta subunitsChad E Grueter
Department of Molecular Physiology and Biophysics, Vanderbilt University Medical Center, Nashville, Tennessee 37232, USA
Biochemistry 47:1760-7. 2008..In combination, these data show that phosphorylation dynamically regulates the interactions of specific isoforms of the Ca2+ channel beta subunits with CaMKII... - Reduced contractile response to alpha1-adrenergic stimulation in atria from mice with chronic cardiac calmodulin kinase II inhibitionMichael Grimm
Institute of Experimental and Clinical Pharmacology and Toxicology, University Medical Center Hamburg Eppendorf, Hamburg, Germany
J Mol Cell Cardiol 42:643-52. 2007..Our data indicate a role of CaMKII in post-rest potentiation and the positive inotropic effect of alpha-adrenergic stimulation at low frequencies... - A calcium sensor in the sodium channel modulates cardiac excitabilityHanno L Tan
Department of Anesthesiology, Vanderbilt University School of Medicine, Nashville 37232, Tennessee, USA
Nature 415:442-7. 2002.... - "We are not alone": ion channel mutations in a long QT syndrome cohortMark E Anderson
Heart Rhythm 2:1106-7. 2005 - Multiple downstream proarrhythmic targets for calmodulin kinase II: moving beyond an ion channel-centric focusMark E Anderson
University of Iowa, Carver College of Medicine, Department of Internal Medicine, 200 Hawkins Drive, E315 A1 GH, Iowa City, IA 52242 USA
Cardiovasc Res 73:657-66. 2007.... - Calmodulin kinase II inhibition shortens action potential duration by upregulation of K+ currentsJingdong Li
Department of Internal Medicine, University of Iowa, Carver College of Medicine, Iowa City, USA
Circ Res 99:1092-9. 2006..These findings provide novel in vivo and cellular evidence that CaMKII links Ca(2+)(i) to cardiac repolarization and suggest that PLN may be a critical CaMKII target for feedback regulation of APD in ventricular myocytes... - The fire from within: the biggest Ca2+ channel erupts and dribblesMark E Anderson
Circ Res 97:1213-5. 2005 - Deciphering the message of long QT genotypesJohn T Kimbrough
J Cardiovasc Electrophysiol 14:1154-5. 2003 - Calcium and stunning: when, from where, and what next?Mark E Anderson
J Cardiovasc Electrophysiol 13:1025-6. 2002 - Suppression of dynamic Ca(2+) transient responses to pacing in ventricular myocytes from mice with genetic calmodulin kinase II inhibitionYuejin Wu
Department of Internal Medicine, Vanderbilt University
J Mol Cell Cardiol 40:213-23. 2006..These findings show that chronic CaMKII inhibition reduces variability of CICR responses in a manner that is partly dependent on the presence of PLN... - Too little, too late: chasing atrial fibrillation with sodium channel antagonistsMark E Anderson
J Cardiovasc Electrophysiol 17:655-6. 2006 - Sudden Infant Death Syndrome and prenatal maternal smoking: rising attributed risk in the Back to Sleep eraMark E Anderson
Department of Community Health Services, Division of Pediatrics, Denver Health and Hospitals Authority, Denver, Colorado, USA
BMC Med 3:4. 2005..This study quantifies the relationship between prenatal smoking and infant death over the time period of the Back to Sleep campaign in the United States, which encouraged parents to use a supine sleeping position for infants... - Calmodulin kinase II inhibition enhances ischemic preconditioning by augmenting ATP-sensitive K+ currentJingdong Li
Departments of Medicine, Carver College of Medicine, University of Iowa, Iowa City, Iowa 52242 1081, USA
Channels (Austin) 1:387-94. 2007..Our study results show CaMKII inhibition enhances beneficial effects of IP by increasing I(KATP)... - Successful school-based intervention for inner-city children with persistent asthmaMark E Anderson
Department of Community Health Services, Denver Health, Denver, Colorado 80204, USA
J Asthma 41:445-53. 2004..This study sought to determine the impact of the Kunsberg program on asthma utilization... - Disease mechanisms and emerging therapies: protein kinases and their inhibitors in myocardial diseaseMark E Anderson
Cardiovascular Research Center at the University of Iowa, Iowa City 52242 1081, USA
Nat Clin Pract Cardiovasc Med 3:437-45. 2006.... - Calmodulin kinase II inhibition disrupts cardiomyopathic effects of enhanced green fluorescent proteinMichelle S C Khoo
Department of Internal Medicine, University of Colorado at Denver and Health Sciences Center, Aurora, CO 80045, USA
J Mol Cell Cardiol 44:405-10. 2008..These findings suggest that increased CaMKII activity is a critical pathological signal in transgenic cardiomyopathy due to eGFP over-expression... - When will we know enough to treat atrial fibrillation?Mark E Anderson
Heart Rhythm 4:750-1. 2007 - MicroRNA may have macro effect on sudden deathMark E Anderson
Nat Med 13:410-1. 2007 - A dynamic pathway for calcium-independent activation of CaMKII by methionine oxidationJeffrey R Erickson
Department of Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City, IA 52242 1109, USA
Cell 133:462-74. 2008..Our data demonstrate a dynamic mechanism for CaMKII activation by oxidation and highlight the critical importance of oxidation-dependent CaMKII activation to AngII and ischemic myocardial apoptosis...