Axel Gödecke

Summary

Affiliation: Heinrich Heine University
Country: Germany

Publications

  1. doi request reprint Intra- and interorgan communication in the cardiovascular system - a special view on redox regulation
    Axel Gödecke
    University of Duesseldorf, Medical Faculty, Duesseldorf, Germany
    Antioxid Redox Signal . 2017
  2. ncbi request reprint Myoglobin protects the heart from inducible nitric-oxide synthase (iNOS)-mediated nitrosative stress
    Axel Gödecke
    Institut für Herz und Kreislaufphysiologie, Heinrich Heine Universitat, Postfach 101007, 40001 Dusseldorf, Germany
    J Biol Chem 278:21761-6. 2003
  3. doi request reprint Nitric oxide-mediated protein modification in cardiovascular physiology and pathology
    Axel Gödecke
    Institut für Herz und Kreislaufphysiologie, Heinrich Heine Universitat, Dusseldorf, Germany
    Proteomics Clin Appl 2:811-22. 2008
  4. ncbi request reprint Adaptive mechanisms of the cardiovascular system in transgenic mice--lessons from eNOS and myoglobin knockout mice
    A Godecke
    Institut für Herz und Kreislaufphysiologie, Heinrich Heine Universitat, Dusseldorf, Germany
    Basic Res Cardiol 95:492-8. 2000
  5. pmc cAMP: fuel for extracellular adenosine formation?
    A Godecke
    Institut für Herz und Kreislaufphysiologie, Heinrich Heine Universitat Dusseldorf, Dusseldorf, Germany
    Br J Pharmacol 153:1087-9. 2008
  6. ncbi request reprint On the impact of NO-globin interactions in the cardiovascular system
    Axel Gödecke
    Institut für Herz und Kreislaufphysiologie, Heinrich Heine Universität Postfach 101007, 40001 Dusseldorf, Germany
    Cardiovasc Res 69:309-17. 2006
  7. ncbi request reprint Endothelial dysfunction of coronary resistance vessels in apoE-/- mice involves NO but not prostacyclin-dependent mechanisms
    Axel Gödecke
    Institut für Herz und Kreislaufphysiologie, Heinrich Heine Universitat Dusseldorf, Postfach 101007, 40001 Dusseldorf, Germany
    Cardiovasc Res 53:253-62. 2002
  8. ncbi request reprint Cardiac-specific overexpression of inducible nitric oxide synthase does not result in severe cardiac dysfunction
    Jacqueline Heger
    Institut für Herz und Kreislaufphysiologie, Heinrich Heine Universitat Dusseldorf, Germany
    Circ Res 90:93-9. 2002
  9. ncbi request reprint Acute inhibition of myoglobin impairs contractility and energy state of iNOS-overexpressing hearts
    Carsten Wunderlich
    Institute for Cardiovascular Physiology, Heinrich Heine University, Dusseldorf, Germany
    Circ Res 92:1352-8. 2003
  10. ncbi request reprint Targeted disruption of cd73/ecto-5'-nucleotidase alters thromboregulation and augments vascular inflammatory response
    Patrycja Koszalka
    Department of Cardiovascular Physiology, Heinrich Heine University Duesseldorf, Duesseldorf, Germany
    Circ Res 95:814-21. 2004

Collaborators

Detail Information

Publications39

  1. doi request reprint Intra- and interorgan communication in the cardiovascular system - a special view on redox regulation
    Axel Gödecke
    University of Duesseldorf, Medical Faculty, Duesseldorf, Germany
    Antioxid Redox Signal . 2017
    ..This forum issue will summarize novel mechanisms involved in intraorgan and interorgan communication of the cardiovascular system, with a special view on the remote organs, skeletal muscle and kidney...
  2. ncbi request reprint Myoglobin protects the heart from inducible nitric-oxide synthase (iNOS)-mediated nitrosative stress
    Axel Gödecke
    Institut für Herz und Kreislaufphysiologie, Heinrich Heine Universitat, Postfach 101007, 40001 Dusseldorf, Germany
    J Biol Chem 278:21761-6. 2003
    ..Our findings indicate that excessive cardiac NO formation can cause heart failure; however, under normal circumstances myoglobin constitutes the important barrier that efficiently protects the heart from nitrosative stress...
  3. doi request reprint Nitric oxide-mediated protein modification in cardiovascular physiology and pathology
    Axel Gödecke
    Institut für Herz und Kreislaufphysiologie, Heinrich Heine Universitat, Dusseldorf, Germany
    Proteomics Clin Appl 2:811-22. 2008
    ....
  4. ncbi request reprint Adaptive mechanisms of the cardiovascular system in transgenic mice--lessons from eNOS and myoglobin knockout mice
    A Godecke
    Institut für Herz und Kreislaufphysiologie, Heinrich Heine Universitat, Dusseldorf, Germany
    Basic Res Cardiol 95:492-8. 2000
    ....
  5. pmc cAMP: fuel for extracellular adenosine formation?
    A Godecke
    Institut für Herz und Kreislaufphysiologie, Heinrich Heine Universitat Dusseldorf, Dusseldorf, Germany
    Br J Pharmacol 153:1087-9. 2008
    ..demonstrate the existence of an extracellular cAMP-adenosine cascade in skeletal muscle cells which suggests a link between adrenergic stimulation of contraction, elevated cAMP formation and release and exercise hyperaemia...
  6. ncbi request reprint On the impact of NO-globin interactions in the cardiovascular system
    Axel Gödecke
    Institut für Herz und Kreislaufphysiologie, Heinrich Heine Universität Postfach 101007, 40001 Dusseldorf, Germany
    Cardiovasc Res 69:309-17. 2006
    ..Members of the globin family of proteins, mainly hemoglobin and myoglobin, have been found to play important roles in all of these processes...
  7. ncbi request reprint Endothelial dysfunction of coronary resistance vessels in apoE-/- mice involves NO but not prostacyclin-dependent mechanisms
    Axel Gödecke
    Institut für Herz und Kreislaufphysiologie, Heinrich Heine Universitat Dusseldorf, Postfach 101007, 40001 Dusseldorf, Germany
    Cardiovasc Res 53:253-62. 2002
    ..We have analyzed the extent of endothelial dysfunction in cardiac resistance vessels of hyperlipidaemic apoE-/- mice and explored whether NO and/or prostacyclin dependent pathways are involved...
  8. ncbi request reprint Cardiac-specific overexpression of inducible nitric oxide synthase does not result in severe cardiac dysfunction
    Jacqueline Heger
    Institut für Herz und Kreislaufphysiologie, Heinrich Heine Universitat Dusseldorf, Germany
    Circ Res 90:93-9. 2002
    ..The concept that iNOS-derived NO is the triggering factor in the pathomechanism leading to heart failure therefore needs to be reevaluated...
  9. ncbi request reprint Acute inhibition of myoglobin impairs contractility and energy state of iNOS-overexpressing hearts
    Carsten Wunderlich
    Institute for Cardiovascular Physiology, Heinrich Heine University, Dusseldorf, Germany
    Circ Res 92:1352-8. 2003
    ..Our findings demonstrate that myoglobin serves as an important cytoplasmic buffer of iNOS-derived NO, which determines the functional consequences of iNOS overexpression...
  10. ncbi request reprint Targeted disruption of cd73/ecto-5'-nucleotidase alters thromboregulation and augments vascular inflammatory response
    Patrycja Koszalka
    Department of Cardiovascular Physiology, Heinrich Heine University Duesseldorf, Duesseldorf, Germany
    Circ Res 95:814-21. 2004
    ....
  11. ncbi request reprint Lack of myoglobin causes a switch in cardiac substrate selection
    Ulrich Flogel
    Institut für Herz und Kreislaufphysiologie, Heinrich Heine Universitat Dusseldorf, Germany
    Circ Res 96:e68-75. 2005
    ..Furthermore, our data suggest that an altered myoglobin level itself may be a critical determinant for substrate selection in the heart. The full text of this article is available online at http://circres.ahajournals.org...
  12. ncbi request reprint Role of myoglobin in the antioxidant defense of the heart
    Ulrich Flogel
    Institut für Herz und Kreislaufphysiologie, Heinrich Heine Universitat Dusseldorf, Universitatsstrasse 1, 40225 Dusseldorf, Germany
    FASEB J 18:1156-8. 2004
    ..We propose that Mb is a key element influencing redox pathways in cardiac muscle to functionally and metabolically protect the heart from oxidative damage...
  13. ncbi request reprint Adenosine produced via the CD73/ecto-5'-nucleotidase pathway has no impact on erythropoietin production but is associated with reduced kidney weight
    Burcin Ozüyaman
    Department of Cardiovascular Physiology, Heinrich Heine University Duesseldorf, Universitaetsstrasse 1, 40225, Duesseldorf, Germany
    Pflugers Arch 452:324-31. 2006
    ..We conclude that adenosine derived by the extracellular CD73 pathway has no impact on EPO production under basal conditions and after hypoxic challenge but may determine kidney weight...
  14. pmc Circulating NOS3 modulates left ventricular remodeling following reperfused myocardial infarction
    Simone Gorressen
    Medical Faculty, Division of Cardiology, Pulmonology and Vascular Medicine, Heinrich Heine University, Dusseldorf, Germany
    PLoS ONE 10:e0120961. 2015
    ..In the current study we hypothesized that circulating NOS3 also affects remodeling of the left ventricle following reperfused MI...
  15. pmc Contribution of cytochrome P450 metabolites to bradykinin-induced vasodilation in endothelial NO synthase deficient mouse hearts
    Zhaoping Ding
    Institut für Herz und Kreislaufphysiologie, Heinrich Heine Universitat Dusseldorf, D 40225 Dusseldorf, Germany
    Br J Pharmacol 135:631-8. 2002
    ..The CYP450 dependent vasodilator was was functionally up-regulated in eNOS-/- hearts and thus likely to compensate for the loss of eNOS in the coronary circulation...
  16. ncbi request reprint Adaptation of the myoglobin knockout mouse to hypoxic stress
    Georg Schlieper
    Department of Cardiovascular Physiology, Heinrich Heine University, 40225 Dusseldorf, Germany
    Am J Physiol Regul Integr Comp Physiol 286:R786-92. 2004
    ..Our data thus demonstrate that myo-/- mice do not decompensate du ing hypoxic st ess but a e surprisingly well adapted. Changes in ene gy metabolism of fatty acids may contribute to the robustness of myoglobin-deficient mice...
  17. ncbi request reprint Endothelial nitric oxide synthase plays a minor role in inhibition of arterial thrombus formation
    Burcin Ozüyaman
    Institut für Herz und Kreislaufphysiologie, Heinrich Heine Universitat, Postfach 101007, 40001 Dusseldorf, Germany
    Thromb Haemost 93:1161-7. 2005
    ..Thus, in the mouse endothelial NO synthase does not play a major role in the autocrine modulation of platelet function and in thrombosis of conduit vessels in vivo...
  18. ncbi request reprint Plasma nitrite reflects constitutive nitric oxide synthase activity in mammals
    Petra Kleinbongard
    Department of Medicine, Division of Cardiology, Pulmonary Diseases, Angiology, Heinrich Heine University, Duesseldorf, Germany
    Free Radic Biol Med 35:790-6. 2003
    ..These results provide evidence for a uniform constitutive vascular NOS-activity across mammalian species...
  19. doi request reprint Myoglobin-deficient mice activate a distinct cardiac gene expression program in response to isoproterenol-induced hypertrophy
    Andrei Molojavyi
    Institut für Herz und Kreislaufphysiologie, Heinrich Heine Universitat Dusseldorf, 40001 Dusseldorf, Germany
    Physiol Genomics 41:137-45. 2010
    ..In summary, our data show a high capacity of myoglobin-deficient mice to adapt to catecholamine induced cardiac stress which is associated with activation of a distinct cardiac gene expression program...
  20. ncbi request reprint In vivo 2D mapping of impaired murine cardiac energetics in NO-induced heart failure
    Ulrich Flogel
    Institut für Herz und Kreislaufphysiologie, Universitatsklinikum Dusseldorf, Heinrich Heine Universitat, Dusseldorf, Germany
    Magn Reson Med 57:50-8. 2007
    ..17 (tg-iNOS(+)/myo(-/-), N = 5, P < 0.05). Future applications will substantially benefit studies on the cause-and-effect relationship between cardiac energetics and function in other genetically well-defined models of heart failure...
  21. pmc Endothelial NOS (NOS3) impairs myocardial function in developing sepsis
    Annette M van de Sandt
    Division of Cardiology, Pneumology and Angiology, Department of Medicine, University Hospital Dusseldorf, Dusseldorf, Germany
    Basic Res Cardiol 108:330. 2013
    ..Significant contribution by inducible NOS (NOS2) during this early phase of sepsis was excluded. Our data suggest that NOS3 relevantly contributes to bioactive NO pool in developing sepsis resulting in impaired cardiac contractility...
  22. pmc Depletion of circulating blood NOS3 increases severity of myocardial infarction and left ventricular dysfunction
    Marc W Merx
    Division of Cardiology, Pneumology and Angiology, Department of Medicine, University Hospital Dusseldorf, Moorenstrasse 5, 40225, Dusseldorf, Germany
    Basic Res Cardiol 109:398. 2014
    ..Reduced infarct size, preserved cardiac function, NO levels in RBC and RBC deformability suggest a modulating role of circulating NOS3 in an acute model of myocardial I/R in chimeric mice...
  23. doi request reprint IGF-IR signaling attenuates the age-related decline of diastolic cardiac function
    Sarah Moellendorf
    Institut für Herz und Kreislaufphysiologie, Universitatsklinikum, Heinrich Heine Universitat Dusseldorf, Dusseldorf, Germany
    Am J Physiol Endocrinol Metab 303:E213-22. 2012
    ..Endogenous IGF-IR signaling is required for conservation of cardiac function of the aging heart, but not for the integrity of cardiac structure and function of young hearts...
  24. ncbi request reprint Vascular transfer of adenovirus is augmented by nitric oxide in the rat heart
    Alexander Sasse
    Institut für Herz und Kreislaufphysiologie, Heinrich Heine University, 40225 Duesseldorf, Germany
    Am J Physiol Heart Circ Physiol 287:H1362-8. 2004
    ..Our findings demonstrate that SNAP and BK effectively increased coronary transfer of adenovirus suggesting that the inverted isolated heart is a suitable model to optimize vascular transfer of virus under standardized conditions...
  25. doi request reprint β-Adrenergic signaling and response to pressure overload in transgenic mice with cardiac-specific overexpression of inducible NO synthase
    Michael Reinartz
    Institut für Herz and Kreislaufphystologie, Heinrich Heine Universitat Dusseldorf, Postfach 101007, 40001 Dusseldorf, Germany
    Nitric Oxide 25:11-21. 2011
    ..Chronic pressure overload induced a similar extent of cardiac hypertrophy in WT and tg-iNOS hearts. LV function, however, was more compromised in tg-iNOS hearts as revealed by a decreased contractility and cardiac output...
  26. ncbi request reprint Cortico-striatal synaptic plasticity in endothelial nitric oxide synthase deficient mice
    Nanuli Doreulee
    Department of Physiology II, Heinrich Heine Universitat, POB 101007, D 40001 Dusseldorf, Germany
    Brain Res 964:159-63. 2003
    ..Impairment of NO-synthesis thus shifts striatal plasticity towards LTD. This indicates a possible involvement of eNOS from endothelia in neuronal modulation...
  27. doi request reprint Nitrosative stress leads to protein glutathiolation, increased s-nitrosation, and up-regulation of peroxiredoxins in the heart
    Michael Reinartz
    Department of Cardiovascular Physiology, Heinrich Heine University Dusseldorf, Universitatsstrasse 1, Dusseldorf D 40225, Germany
    J Biol Chem 283:17440-9. 2008
    ..Furthermore, S-nitrosation of Prxs may serve a new function in the signaling cascade of nitrosative stress...
  28. ncbi request reprint Detection of TAP-tagged proteins in Western blot, confocal laser scanning microscopy and FACS using the ZZ-domain
    Stephan Weser
    Institut für Herz und Kreislaufphysiologie, Heinrich Heine Universitat Dusseldorf, Postfach 101007, 40001 Dusseldorf, Germany
    J Biochem Biophys Methods 68:189-94. 2006
    ..Thus, we present valuable tools for the analysis of recombinant proteins on the basis of IgG-ZZ interactions, which can be used even if target specific first antibodies are not available or lack sufficient specificity...
  29. ncbi request reprint Coronary hemodynamics in endothelial NO synthase knockout mice
    A Godecke
    Institut für Herz und Kreislaufphysiologie, Heinrich Heine Universitat, Dusseldorf, Germany
    Circ Res 82:186-94. 1998
    ....
  30. ncbi request reprint Titin-Based Cardiac Myocyte Stiffening Contributes to Early Adaptive Ventricular Remodeling After Myocardial Infarction
    Sebastian Kötter
    From the Department of Cardiovascular Physiology S K, M K, C A, K B, A H, A G, M K, Department of Pharmacology and Clinical Pharmacology M G, S G, J W F, J P S, and Institute of Biochemistry and Molecular Biology II J M M, J S, Medical Faculty, Heinrich Heine University Dusseldorf, Germany
    Circ Res 119:1017-1029. 2016
    ..Understanding the mechanisms that support cardiac function in the early phase post MI and identifying the processes that initiate transition to maladaptive remodeling are of major clinical interest...
  31. doi request reprint Expression of the murine Nr4a1 gene is controlled by three distinct genomic loci
    Torben Soker
    Institut für Herz und Kreislaufphysiologie, Heinrich Heine Universitat, Universitatsklinikum Dusseldorf, D 40225 Dusseldorf, Germany
    Gene 512:517-20. 2013
    ..5 kb from the first coding exon. Whereas in HL-1 cells only two of the three distinct transcripts were induced by cAMP, in the heart all transcripts were regulated in response to β-adrenergic stimulation...
  32. doi request reprint Thrombin-induced ATP release from human umbilical vein endothelial cells
    Stefanie Gödecke
    Department of Cardiovascular Physiology, Heinrich Heine University, Dusseldorf, Germany
    Am J Physiol Cell Physiol 302:C915-23. 2012
    ..ATP is released by a carbenoxolone- and Gd(3+)- sensitive pathway, most likely involving Panx1 channels...
  33. pmc Inotropic response to beta-adrenergic receptor stimulation and anti-adrenergic effect of ACh in endothelial NO synthase-deficient mouse hearts
    A Godecke
    Institut für Herz und Kreislauf physiologie, Heinrich Heine Universitat Dusseldorf, Germany
    J Physiol 532:195-204. 2001
    ....
  34. pmc Disruption of myoglobin in mice induces multiple compensatory mechanisms
    A Godecke
    Institut für Herz und Kreislaufphysiologie, Heinrich Heine Universitat Dusseldorf, Postfach 101007, 40001 Dusseldorf, Germany
    Proc Natl Acad Sci U S A 96:10495-500. 1999
    ....
  35. doi request reprint Impact of dietary nitrate on age-related diastolic dysfunction
    Christos Rammos
    West German Heart and Vascular Center Essen, Department of Medicine, Division of Cardiology, Medical Faculty, University Hospital Essen, Essen, Germany
    Eur J Heart Fail 18:599-610. 2016
    ..Whether replenishment of NO deficiency with dietary inorganic nitrate would offer a novel approach to reverse age-related cardiovascular alterations was not known...
  36. ncbi request reprint Mice deficient in endothelial nitric oxide synthase exhibit a selective deficit in hippocampal long-term potentiation
    R I Wilson
    Institut fur Neurophysiologie, Heinrich Heine Universitat, Dusseldorf, Germany
    Neuroscience 90:1157-65. 1999
    ..These results support a selective role for endothelial nitric oxide synthase in long-term potentiation, but also demonstrate that nitric oxide synthase is not involved in this process under all conditions...
  37. pmc Systematic Analysis Reveals Elongation Factor 2 and α-Enolase as Novel Interaction Partners of AKT2
    Katharina Bottermann
    Department of Cardiovascular Physiology, Heinrich Heine University Dusseldorf, Dusseldorf, Germany
    PLoS ONE 8:e66045. 2013
    ..Taken together, these findings point to new aspects of AKT2-mediated signal transduction in protein synthesis and glucose metabolism. ..
  38. ncbi request reprint Protein kinase A- and C-dependent modulation of murine inducible nitric oxide synthase
    T Ishibashi
    Institut für Herz und Kreislaufphysiologie, Heinrich Heine Universitat Dusseldorf, Federal Republic of Germany
    Tohoku J Exp Med 194:75-90. 2001
    ..However, PKA and PKC would possibly modify NOS activity indirectly via cofactors necessary for NO formation...
  39. ncbi request reprint Cloning of the rat P2u receptor and its potential role in coronary vasodilation
    S Gödecke
    Institut für Herz und Kreislaufphysiologie, Heinrich Heine Universitat, Dusseldorf, Germany
    Am J Physiol 270:C570-7. 1996
    ..Our experiments suggest that, in the rat heart, endothelial P2u receptors are involved in the ATP/UTP-mediated vasodilation of coronary blood vessels...