Steven M Pogwizd

Summary

Affiliation: University of Illinois at Chicago
Country: USA

Publications

  1. ncbi request reprint Calcium cycling in heart failure: the arrhythmia connection
    Steven M Pogwizd
    Department of Medicine, University of Illinois at Chicago, USA
    J Cardiovasc Electrophysiol 13:88-91. 2002
  2. ncbi request reprint Intracellular Na in animal models of hypertrophy and heart failure: contractile function and arrhythmogenesis
    Steven M Pogwizd
    Department of Medicine, University of Illinois at Chicago, 840 South Wood Street, M C 787, Chicago, IL 60612, USA
    Cardiovasc Res 57:887-96. 2003
  3. ncbi request reprint Cellular basis of triggered arrhythmias in heart failure
    Steven M Pogwizd
    Steven M Pogwizd is at the Department of Medicine, University of Illinois at Chicago, Chicago, Illinois 60153, USA
    Trends Cardiovasc Med 14:61-6. 2004
  4. ncbi request reprint Ca2+/calmodulin-dependent protein kinase modulates cardiac ryanodine receptor phosphorylation and sarcoplasmic reticulum Ca2+ leak in heart failure
    Xun Ai
    Department of Medicine, University of Illinois at Chicago, IL 60612, USA
    Circ Res 97:1314-22. 2005
  5. ncbi request reprint Intra-sarcoplasmic reticulum free [Ca2+] and buffering in arrhythmogenic failing rabbit heart
    Tao Guo
    Department of Physiology, Loyola University Chicago, Stritch School of Medicine, Maywood, IL 60153, USA
    Circ Res 101:802-10. 2007
  6. ncbi request reprint Clinical potential of sodium-calcium exchanger inhibitors as antiarrhythmic agents
    Steven M Pogwizd
    Department of Medicine, University of Illinois at Chicago, 8430 South Wood Street, Chicago, IL 60612, USA
    Drugs 63:439-52. 2003
  7. pmc Connexin43 knockdown or overexpression modulates cell coupling in control and failing rabbit left ventricular myocytes
    Xun Ai
    Division of Cardiovascular Disease, Department of Medicine, UAB Center for Cardiovascular Biology, University of Alabama at Birmingham, 1670 University Boulevard, Volker Hall B140, Birmingham, AL 35294, USA
    Cardiovasc Res 85:751-62. 2010
  8. pmc Enhanced activation of p21-activated kinase 1 in heart failure contributes to dephosphorylation of connexin 43
    Xun Ai
    Department of Medicine, University of Alabama at Birmingham, 1670, University Blvd, Birmingham, AL, USA
    Cardiovasc Res 92:106-14. 2011
  9. ncbi request reprint Na/Ca exchange in heart failure: contractile dysfunction and arrhythmogenesis
    Steven M Pogwizd
    Department of Medicine, University of Illinois at Chicago, Chicago, Illinois 60612, USA
    Ann N Y Acad Sci 976:454-65. 2002
  10. pmc Isoform- and tissue-specific regulation of the Ca(2+)-sensitive transcription factor NFAT in cardiac myocytes and heart failure
    Andreas Rinne
    Dept of Molecular Biophysics and Physiology, RUSH Univ Medical Center, 1750 W Harrison St, Chicago, IL 60612, USA
    Am J Physiol Heart Circ Physiol 298:H2001-9. 2010

Collaborators

Detail Information

Publications28

  1. ncbi request reprint Calcium cycling in heart failure: the arrhythmia connection
    Steven M Pogwizd
    Department of Medicine, University of Illinois at Chicago, USA
    J Cardiovasc Electrophysiol 13:88-91. 2002
    ..It is imperative that therapeutic approaches for ventricular tachycardia in HF take into consideration cellular Ca handling and excitation-contractile coupling, and their alteration in the failing heart...
  2. ncbi request reprint Intracellular Na in animal models of hypertrophy and heart failure: contractile function and arrhythmogenesis
    Steven M Pogwizd
    Department of Medicine, University of Illinois at Chicago, 840 South Wood Street, M C 787, Chicago, IL 60612, USA
    Cardiovasc Res 57:887-96. 2003
  3. ncbi request reprint Cellular basis of triggered arrhythmias in heart failure
    Steven M Pogwizd
    Steven M Pogwizd is at the Department of Medicine, University of Illinois at Chicago, Chicago, Illinois 60153, USA
    Trends Cardiovasc Med 14:61-6. 2004
    ....
  4. ncbi request reprint Ca2+/calmodulin-dependent protein kinase modulates cardiac ryanodine receptor phosphorylation and sarcoplasmic reticulum Ca2+ leak in heart failure
    Xun Ai
    Department of Medicine, University of Illinois at Chicago, IL 60612, USA
    Circ Res 97:1314-22. 2005
    ..Our results suggest that CaMKII-dependent phosphorylation of RyR2 is involved in enhanced SR diastolic Ca leak and reduced SR Ca load in HF, and may thus contribute to arrhythmias and contractile dysfunction in HF...
  5. ncbi request reprint Intra-sarcoplasmic reticulum free [Ca2+] and buffering in arrhythmogenic failing rabbit heart
    Tao Guo
    Department of Physiology, Loyola University Chicago, Stritch School of Medicine, Maywood, IL 60153, USA
    Circ Res 101:802-10. 2007
    ..We conclude that low total SR Ca2+ content in HF, and reduced SR Ca2+ release, is attributable to reduced [Ca2+]SR, not to alterations in SR volume or Ca2+ buffering capacity...
  6. ncbi request reprint Clinical potential of sodium-calcium exchanger inhibitors as antiarrhythmic agents
    Steven M Pogwizd
    Department of Medicine, University of Illinois at Chicago, 8430 South Wood Street, Chicago, IL 60612, USA
    Drugs 63:439-52. 2003
    ....
  7. pmc Connexin43 knockdown or overexpression modulates cell coupling in control and failing rabbit left ventricular myocytes
    Xun Ai
    Division of Cardiovascular Disease, Department of Medicine, UAB Center for Cardiovascular Biology, University of Alabama at Birmingham, 1670 University Boulevard, Volker Hall B140, Birmingham, AL 35294, USA
    Cardiovasc Res 85:751-62. 2010
    ..However, the role of Cx43 downregulation per se in impaired coupling in HF is unclear...
  8. pmc Enhanced activation of p21-activated kinase 1 in heart failure contributes to dephosphorylation of connexin 43
    Xun Ai
    Department of Medicine, University of Alabama at Birmingham, 1670, University Blvd, Birmingham, AL, USA
    Cardiovasc Res 92:106-14. 2011
    ..Here, we further explore the molecular mechanisms of enhanced dephosphorylation of Cx43 in HF. p21-activated kinase 1 (PAK1) is a serine-threonine protein kinase that has been shown to activate PP2A...
  9. ncbi request reprint Na/Ca exchange in heart failure: contractile dysfunction and arrhythmogenesis
    Steven M Pogwizd
    Department of Medicine, University of Illinois at Chicago, Chicago, Illinois 60612, USA
    Ann N Y Acad Sci 976:454-65. 2002
    ..Therapeutic approaches to the treatment of HF will need to balance increasing SR Ca load with the arrhythmogenic effects of SR Ca overload that involve activation of I(ti) carried by Na/Ca exchanger...
  10. pmc Isoform- and tissue-specific regulation of the Ca(2+)-sensitive transcription factor NFAT in cardiac myocytes and heart failure
    Andreas Rinne
    Dept of Molecular Biophysics and Physiology, RUSH Univ Medical Center, 1750 W Harrison St, Chicago, IL 60612, USA
    Am J Physiol Heart Circ Physiol 298:H2001-9. 2010
    ..We conclude that the activation of NFAT in adult cardiomyocytes is isoform and tissue specific and is tightly controlled by nuclear export. NFAT is activated in myocytes from HF animals and may be secondary to Ca(2+) overload...
  11. ncbi request reprint Connexin 43 downregulation and dephosphorylation in nonischemic heart failure is associated with enhanced colocalized protein phosphatase type 2A
    Xun Ai
    Department of Medicine, University of Illinois at Chicago, IL 60612, USA
    Circ Res 96:54-63. 2005
    ..Increased levels of PP2A that colocalize with Cx43 can underlie enhanced levels of Cx43-NP in HF. Modulation of Cx43 phosphorylation may be a potential therapeutic target to improve conduction in HF...
  12. ncbi request reprint Elevated sarcoplasmic reticulum Ca2+ leak in intact ventricular myocytes from rabbits in heart failure
    Thomas R Shannon
    Department of Molecular Biophysics and Physiology, Rush University, 1750 W Harrison Ave, Chicago, Ill 60612, USA
    Circ Res 93:592-4. 2003
    ..We conclude that increased diastolic SR Ca2+ leak in HF may contribute to reductions in SR Ca2+ content, but changes in NCX in this HF model have more impact on [Ca2+]SRT...
  13. ncbi request reprint Creating a cardiac pacemaker by gene therapy
    Traian M Anghel
    Department of Medicine, Section of Cardiology, University of Illinois at Chicago, Chicago, IL 60612, USA
    Med Biol Eng Comput 45:145-55. 2007
    ..Additional requirements and refinements necessary for successful biopacemaker function by gene transfer are discussed...
  14. doi request reprint Focal initiation of sustained and nonsustained ventricular tachycardia in a canine model of ischemic cardiomyopathy
    Carolyn M Johnson
    Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA
    J Cardiovasc Electrophysiol 23:543-52. 2012
    ....
  15. ncbi request reprint Micropatterns of propagation
    Peter J Lee
    University of Illinois at Chicago, 60612 7323, USA
    Adv Cardiol 42:86-106. 2006
    ....
  16. ncbi request reprint Gene therapy to develop a genetically engineered cardiac pacemaker
    Christopher M Glenn
    Department of Medicine, University of Illinois at Chicago, Chicago, Ill 60612, USA
    J Cardiovasc Nurs 18:330-6. 2003
    ....
  17. pmc Activation becomes highly organized during long-duration ventricular fibrillation in canine hearts
    Li Li
    Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA
    Am J Physiol Heart Circ Physiol 298:H2046-53. 2010
    ..PFs appear to play an important role during this stage of VF...
  18. pmc Sex differences in repolarization and slow delayed rectifier potassium current and their regulation by sympathetic stimulation in rabbits
    Yujie Zhu
    Department of Medicine, University of Alabama at Birmingham, 1670 University Blvd, Birmingham, AL 35294, USA
    Pflugers Arch 465:805-18. 2013
    ..01). In conclusion, we found that there are sex differences in IKs, AP, and their regulation by β-AR's that are modulated by sex hormones, suggesting the potential for sex-specific antiarrhythmic therapy...
  19. ncbi request reprint Increased expression of alternatively spliced dominant-negative isoform of SRF in human failing hearts
    Francesca J Davis
    Department of Surgery Cardiac and Thoracic, University of Chicago, Illinois 60637, USA
    Am J Physiol Heart Circ Physiol 282:H1521-33. 2002
    ..These results suggest that expression of SRF-Delta4,5 in failing hearts may in part contribute to impaired cardiac gene expression and consequently to the pathogenesis of heart failure...
  20. ncbi request reprint Intracellular Na(+) concentration is elevated in heart failure but Na/K pump function is unchanged
    Sanda Despa
    Department of Physiology, Loyola University Chicago, Maywood, IL 60153, USA
    Circulation 105:2543-8. 2002
    ..Intracellular sodium concentration ([Na(+)](i)) modulates cardiac contractile and electrical activity through Na/Ca exchange (NCX). Upregulation of NCX in heart failure (HF) may magnify the functional impact of altered [Na(+)](i)...
  21. ncbi request reprint Upregulated Na/Ca exchange is involved in both contractile dysfunction and arrhythmogenesis in heart failure
    Donald M Bers
    Department of Physiology, Loyola University Chicago, 2160 South First Avenue, Maywood, IL 60153, USA
    Basic Res Cardiol 97:I36-42. 2002
    ..We conclude that NaCaX contributes in major ways to both contractile dysfunction (by reducing SR Ca) and increased propensity for triggered arrhythmias (by increasing I(ti) and DADs)...
  22. ncbi request reprint Adenoviral gene transfer of mutant phospholamban rescues contractile dysfunction in failing rabbit myocytes with relatively preserved SERCA function
    Mark T Ziolo
    Department of Physiology, Loyola University Chicago, Maywood, Ill, USA
    Circ Res 96:815-7. 2005
    ..This approach could enhance contractile function in failing hearts of various etiologies, even here where reduced SERCA activity is not the main dysfunction...
  23. pmc Arrhythmogenic effects of beta2-adrenergic stimulation in the failing heart are attributable to enhanced sarcoplasmic reticulum Ca load
    Jaime DeSantiago
    Department of Pharmacology, University of California Davis, Davis, CA, USA
    Circ Res 102:1389-97. 2008
    ..Thus, beta(2)-AR stimulation is arrhythmogenic in HF, mediated by SR Ca overload-induced spontaneous SR Ca release and aftercontractions...
  24. doi request reprint Ca2+/calmodulin-dependent protein kinase IIdelta and protein kinase D overexpression reinforce the histone deacetylase 5 redistribution in heart failure
    Julie Bossuyt
    Department of Physiology, Loyola University Chicago, Maywood, IL 60153, USA
    Circ Res 102:695-702. 2008
    ..This may directly contribute to the development and/or maintenance of HF...
  25. ncbi request reprint Noninvasive three-dimensional electrocardiographic imaging of ventricular activation sequence
    Xin Zhang
    Dept of Biomedical Engineering, Univ of Minnesota, 7 105 BSBE, 312 Church St, Minneapolis, MN 55455, USA
    Am J Physiol Heart Circ Physiol 289:H2724-32. 2005
    ..This new 3-D electrocardiographic imaging modality has the potential to guide catheter-based ablative interventions for the treatment of life-threatening cardiac arrhythmias...
  26. ncbi request reprint Three-dimensional myocardial activation imaging in a rabbit model
    Chenguang Liu
    University of Minnesota, Minneapolis 55455, USA
    IEEE Trans Biomed Eng 53:1813-20. 2006
    ..20 and the localization error was 5.1 mm. The present simulation and experimental results suggest the merits of the 3DECI imaging approach, and the validity of intracardiac mapping as a tool to evaluate the 3DECI...
  27. pmc Intracellular [Na+] and Na+ pump rate in rat and rabbit ventricular myocytes
    Sanda Despa
    Department of Physiology and Cardiovascular Institute, Loyola University Chicago, Maywood, IL 60153, USA
    J Physiol 539:133-43. 2002
    ..We conclude that resting [Na+]i is higher in rat than in rabbit, that this is caused by higher resting Na+ influx in rat and that a higher Na+,K+-ATPase pumping rate in rat is a consequence of the higher [Na+]i...
  28. ncbi request reprint Expression and phosphorylation of the na-pump regulatory subunit phospholemman in heart failure
    Julie Bossuyt
    Department of Physiology, Loyola University Chicago, Maywood, IL 60153, USA
    Circ Res 97:558-65. 2005
    ..So reduced Na/K-ATPase expression in HF may be functionally offset by lower inhibition by PLM (because of reduced PLM expression and higher PLM phosphorylation)...