K C Wollert

Summary

Affiliation: Hannover Medical School
Country: Germany

Publications

  1. doi request reprint Growth differentiation factor 15 in heart failure: an update
    Kai C Wollert
    Division of Molecular and Translational Cardiology, Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany
    Curr Heart Fail Rep 9:337-45. 2012
  2. ncbi request reprint Clinical applications of stem cells for the heart
    Kai C Wollert
    Department of Cardiology and Angiology, Hanover Medical School, Hanover, Germany
    Circ Res 96:151-63. 2005
  3. doi request reprint Cell therapy for acute myocardial infarction
    Kai C Wollert
    Department of Cardiology and Angiology, Hannover University Medical School, Carl Neuberg Str 1, 30625 Hannover, Germany
    Curr Opin Pharmacol 8:202-10. 2008
  4. doi request reprint Cell therapy for the treatment of coronary heart disease: a critical appraisal
    Kai C Wollert
    Hans Borst Center for Heart and Stem Cell Research, Department of Cardiology and Angiology, Hannover Medical School, 30625 Hannover, Germany
    Nat Rev Cardiol 7:204-15. 2010
  5. ncbi request reprint Regulation of cardiac remodeling by nitric oxide: focus on cardiac myocyte hypertrophy and apoptosis
    Kai C Wollert
    Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany
    Heart Fail Rev 7:317-25. 2002
  6. ncbi request reprint Prognostic value of growth-differentiation factor-15 in patients with non-ST-elevation acute coronary syndrome
    Kai C Wollert
    Department of Cardiology and Angiology, Hannover Medical School, Germany
    Circulation 115:962-71. 2007
  7. ncbi request reprint Gene transfer of cGMP-dependent protein kinase I enhances the antihypertrophic effects of nitric oxide in cardiomyocytes
    Kai C Wollert
    Department of Cardiology and Angiology, Medizinische Hochschule Hannover, Hannover, Germany
    Hypertension 39:87-92. 2002
  8. ncbi request reprint The role of interleukin-6 in the failing heart
    K C Wollert
    Department of Cardiology and Angiology, Medizinische Hochschule Hannover, Carl Neuberg Str 1, 30625 Hannover, Germany
    Heart Fail Rev 6:95-103. 2001
  9. ncbi request reprint The renin-angiotensin system and experimental heart failure
    K C Wollert
    Department of Cardiology and Angiology, Medizinische Hochschule Hannover, Germany
    Cardiovasc Res 43:838-49. 1999
  10. pmc Inhibition of calcineurin-NFAT hypertrophy signaling by cGMP-dependent protein kinase type I in cardiac myocytes
    Beate Fiedler
    Department of Cardiology and Angiology, Hannover Medical School, 30625 Hannover, Germany
    Proc Natl Acad Sci U S A 99:11363-8. 2002

Detail Information

Publications62

  1. doi request reprint Growth differentiation factor 15 in heart failure: an update
    Kai C Wollert
    Division of Molecular and Translational Cardiology, Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany
    Curr Heart Fail Rep 9:337-45. 2012
    ..Further understanding of the pathobiology of GDF-15 may lead to the discovery of new treatment targets in HF...
  2. ncbi request reprint Clinical applications of stem cells for the heart
    Kai C Wollert
    Department of Cardiology and Angiology, Hanover Medical School, Hanover, Germany
    Circ Res 96:151-63. 2005
    ..At the same time, continued basic research to elucidate the underlying mechanism of stem cell therapy is clearly needed...
  3. doi request reprint Cell therapy for acute myocardial infarction
    Kai C Wollert
    Department of Cardiology and Angiology, Hannover University Medical School, Carl Neuberg Str 1, 30625 Hannover, Germany
    Curr Opin Pharmacol 8:202-10. 2008
    ....
  4. doi request reprint Cell therapy for the treatment of coronary heart disease: a critical appraisal
    Kai C Wollert
    Hans Borst Center for Heart and Stem Cell Research, Department of Cardiology and Angiology, Hannover Medical School, 30625 Hannover, Germany
    Nat Rev Cardiol 7:204-15. 2010
    ..The identification of reliable sources of pluripotent stem cells and their differentiation into mature cardiac cell types could ultimately enable regeneration of the infarcted heart...
  5. ncbi request reprint Regulation of cardiac remodeling by nitric oxide: focus on cardiac myocyte hypertrophy and apoptosis
    Kai C Wollert
    Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany
    Heart Fail Rev 7:317-25. 2002
    ..In the future, these novel insights into the role of NO in cardiac remodeling should allow the development of novel therapeutic strategies to treat cardiac remodeling and failure...
  6. ncbi request reprint Prognostic value of growth-differentiation factor-15 in patients with non-ST-elevation acute coronary syndrome
    Kai C Wollert
    Department of Cardiology and Angiology, Hannover Medical School, Germany
    Circulation 115:962-71. 2007
    ..Circulating levels of GDF-15 may provide prognostic information in patients with non-ST-elevation acute coronary syndrome...
  7. ncbi request reprint Gene transfer of cGMP-dependent protein kinase I enhances the antihypertrophic effects of nitric oxide in cardiomyocytes
    Kai C Wollert
    Department of Cardiology and Angiology, Medizinische Hochschule Hannover, Hannover, Germany
    Hypertension 39:87-92. 2002
    ..Adenoviral gene transfer of PKG I selectively enhances the antihypertrophic effects of NO without increasing the susceptibility to apoptosis...
  8. ncbi request reprint The role of interleukin-6 in the failing heart
    K C Wollert
    Department of Cardiology and Angiology, Medizinische Hochschule Hannover, Carl Neuberg Str 1, 30625 Hannover, Germany
    Heart Fail Rev 6:95-103. 2001
    ..This review summarizes clinical and experimental data from this rapidly evolving field, which, taken together, strongly suggest that IL-6 and IL-6 related cytokines are intricately involved in the pathophysiology of the failing heart...
  9. ncbi request reprint The renin-angiotensin system and experimental heart failure
    K C Wollert
    Department of Cardiology and Angiology, Medizinische Hochschule Hannover, Germany
    Cardiovasc Res 43:838-49. 1999
    ..In this paper, we review recent experimental evidence suggesting a critical role for the RAS in cardiac hypertrophy and failure with special emphasis on the putative role of Ang II and Ang II-receptor signaling in cardiac myocytes...
  10. pmc Inhibition of calcineurin-NFAT hypertrophy signaling by cGMP-dependent protein kinase type I in cardiac myocytes
    Beate Fiedler
    Department of Cardiology and Angiology, Hannover Medical School, 30625 Hannover, Germany
    Proc Natl Acad Sci U S A 99:11363-8. 2002
    ..Inhibition of calcineurin-NFAT signaling by PKG I provides a framework for understanding how NO inhibits cardiac myocyte hypertrophy...
  11. ncbi request reprint Downregulation of cytoskeletal muscle LIM protein by nitric oxide: impact on cardiac myocyte hypertrophy
    Jörg Heineke
    Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany
    Circulation 107:1424-32. 2003
    ..We postulated that NO modulates expression of genes in cardiac myocytes that may be functionally important in the context of cardiac hypertrophy and failure...
  12. doi request reprint Potential novel pharmacological therapies for myocardial remodelling
    Ulf Landmesser
    Deparment of Cardiology and Angiology, Hannover Medical School, Carl Neuberg Str 1, 30625 Hannover, Germany
    Cardiovasc Res 81:519-27. 2009
    ....
  13. ncbi request reprint Regulation of proangiogenic factor CCN1 in cardiac muscle: impact of ischemia, pressure overload, and neurohumoral activation
    Denise Hilfiker-Kleiner
    Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany
    Circulation 109:2227-33. 2004
    ..Because these conditions occur in myocardial ischemia and pressure overload, we investigated the regulation of CCN1 in cardiomyocytes in vitro and in the heart in vivo...
  14. pmc Attenuation of cardiac remodeling after myocardial infarction by muscle LIM protein-calcineurin signaling at the sarcomeric Z-disc
    Joerg Heineke
    Department of Cardiology, Hanover Medical School, 30625 Hanover, Germany
    Proc Natl Acad Sci U S A 102:1655-60. 2005
    ..Our study reveals a link between the stress sensor MLP and the calcineurin-NFAT pathway at the sarcomeric Z-disk in cardiomyocytes and indicates that reduced MLP-calcineurin signaling predisposes to adverse remodeling after MI...
  15. ncbi request reprint Monitoring of bone marrow cell homing into the infarcted human myocardium
    Michael Hofmann
    Department of Nuclear Medicine, Hanover Medical School, Hanover, Germany
    Circulation 111:2198-202. 2005
    ..Although the mechanisms of this effect remain to be established, homing of BMCs into the infarcted myocardium is probably a critical early event...
  16. ncbi request reprint Haeme oxygenase promotes progenitor cell mobilization, neovascularization, and functional recovery after critical hindlimb ischaemia in mice
    Jörn Tongers
    Department of Cardiology and Angiology, Hannover University Medical School, 30625 Hannover, Germany
    Cardiovasc Res 78:294-300. 2008
    ..We postulated that haeme oxygenase (HO) is required for progenitor cell recruitment, neovascularization, and blood flow recovery after critical hindlimb ischaemia (HLI)...
  17. pmc Increased effects of C-type natriuretic peptide on contractility and calcium regulation in murine hearts overexpressing cyclic GMP-dependent protein kinase I
    Kai C Wollert
    Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany
    Br J Pharmacol 140:1227-36. 2003
    ..cGMP/PKG I-stimulated phosphorylation of PLB and subsequent activation of the sarcoplasmic reticulum Ca2+ pump appear to mediate the positive inotropic and lusitropic responses to CNP...
  18. ncbi request reprint Bone-marrow-derived cell transfer after ST-elevation myocardial infarction: lessons from the BOOST trial
    Helmut Drexler
    Department of Cardiology and Angiology at Hannover Medical School, Hannover, Germany
    Nat Clin Pract Cardiovasc Med 3:S65-8. 2006
    ....
  19. ncbi request reprint The role of stem cells in the post-MI patient
    Gerd P Meyer
    Department of Cardiology and Angiology, Hannover Medical School, Carl Neuberg Str 1, 30625 Hannover, Germany
    Curr Heart Fail Rep 4:198-203. 2007
    ..Ultimately, large outcome trials will be needed. At the same time, continued basic research is needed to elucidate the underlying mechanism of stem cell therapy...
  20. ncbi request reprint Intracoronary bone marrow cell transfer after myocardial infarction: eighteen months' follow-up data from the randomized, controlled BOOST (BOne marrOw transfer to enhance ST-elevation infarct regeneration) trial
    Gerd P Meyer
    Department of Cardiology, Hannover Medical School, Hannover, Germany
    Circulation 113:1287-94. 2006
    ..The critical question of whether BMC transfer can have a sustained impact on LV function remains unanswered...
  21. ncbi request reprint Impact of intracoronary bone marrow cell transfer on diastolic function in patients after acute myocardial infarction: results from the BOOST trial
    Arnd Schaefer
    Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany
    Eur Heart J 27:929-35. 2006
    ..However, the impact of BMC therapy on LV diastolic function in patients after AMI has remained uncertain...
  22. ncbi request reprint Reassessing guidelines for heart failure
    Helmut Drexler
    Chief Cardiovascular Division, Medical University of Hanover, 30625, Germany
    J Renin Angiotensin Aldosterone Syst 5:S28-33. 2004
    ..The selective aldosterone receptor blocker eplerenone was evaluated in the EPHESUS trial in post-MI patients with signs of heart failure. Based on these clinical trials, heart failure guidelines are now being updated...
  23. ncbi request reprint TNFalpha decreases alphaMHC expression by a NO mediated pathway: role of E-box transcription factors for cardiomyocyte specific gene regulation
    Denise Hilfiker-Kleiner
    Department of Cardiology and Angiology, Medizinische Hochschule Hannover, Carl Neuberg Strasse 1, 30625 Hannover, Germany
    Cardiovasc Res 53:460-9. 2002
    ..It is not clear, however, whether TNFalpha mediated NO release has sustained cardiac effects, by altering expression of cardiomyocyte specific genes such as alpha-myosin heavy chain (alphaMHC)...
  24. ncbi request reprint Single L-type Ca(2+) channel regulation by cGMP-dependent protein kinase type I in adult cardiomyocytes from PKG I transgenic mice
    Frank Schroder
    Department of Cardiology and Angiology, Hannover Medical School, Carl Neuberg Str 1, 30625 Hannover, Germany
    Cardiovasc Res 60:268-77. 2003
    ..Both nitric oxide (NO), signaling via cGMP, and acetylcholine, signaling via the muscarinic receptor, have been identified as negative regulators of beta-adrenoreceptor-stimulated LTCC activity in cardiac myocytes...
  25. doi request reprint Long-term effects of intracoronary bone marrow cell transfer on diastolic function in patients after acute myocardial infarction: 5-year results from the randomized-controlled BOOST trial--an echocardiographic study
    Arnd Schaefer
    Clinic of Cardiology and Angiology, Hannover Medical School, Carl Neuberg Strasse 1, Hannover, Germany
    Eur J Echocardiogr 11:165-71. 2010
    ..Therefore, we conducted a 5-year follow-up of the BOOST trial to evaluate a sustained benefit on echocardiographic parameters on diastolic function...
  26. pmc Calcineurin protects the heart in a murine model of dilated cardiomyopathy
    Joerg Heineke
    Department of Pediatrics, University of Cincinnati, Cincinnati Children s Hospital Medical Center, Howard Hughes Medical Institute, 240 Albert Sabin Way, Cincinnati, OH 45229, USA
    J Mol Cell Cardiol 48:1080-7. 2010
    ..Collectively, these results reveal an important and previously unrecognized protective function of endogenous myocardial calcineurin in a mouse model of dilated cardiomyopathy...
  27. doi request reprint Intracoronary bone marrow cell transfer after myocardial infarction: 5-year follow-up from the randomized-controlled BOOST trial
    Gerd P Meyer
    Department of Cardiology and Angiology, Hannover Medical School, Carl Neuberg Str 1, 30625 Hannover, Germany
    Eur Heart J 30:2978-84. 2009
    ..As previously reported, BMC transfer led to an improvement of LVEF by 6.0% at 6 months (P = 0.003) and 2.8% at 18 months (P = 0.27)...
  28. ncbi request reprint Intracoronary autologous bone-marrow cell transfer after myocardial infarction: the BOOST randomised controlled clinical trial
    Kai C Wollert
    Department of Cardiology, Hanover Medical School, Hanover, Germany
    Lancet 364:141-8. 2004
    ..In this randomised trial, we aimed to assess whether intracoronary transfer of autologous bone-marrow cells could improve global left-ventricular ejection fraction (LVEF) at 6 months' follow-up...
  29. ncbi request reprint JunD attenuates phenylephrine-mediated cardiomyocyte hypertrophy by negatively regulating AP-1 transcriptional activity
    Denise Hilfiker-Kleiner
    Department of Cardiology and Angiology, Hannover Medical School, Carl Neuberg Str 1, 30625 Hannover, Germany
    Cardiovasc Res 71:108-17. 2006
    ..In the present study we analyzed the mechanistic role of JunD in cardiomyocyte hypertrophy in vitro in response to alpha-adrenergic agonist phenylephrine (PE)...
  30. doi request reprint Bone marrow cells are a rich source of growth factors and cytokines: implications for cell therapy trials after myocardial infarction
    Mortimer Korf-Klingebiel
    Department of Cardiology and Angiology, Hannover Medical School, Carl Neuberg Str 1, 30625 Hannover, Germany
    Eur Heart J 29:2851-8. 2008
    ..Release of paracrine factors has been proposed as a mechanism for these therapeutic effects; however, this hypothesis has not been tested in humans...
  31. ncbi request reprint Src family tyrosine kinases inhibit single L-type: Ca2+ channel activity in human atrial myocytes
    Frank Schroder
    Department of Cardiology and Angiology, Hannover Medical School, Carl Neuberg Strasse 1, Hannover 30625, Germany
    J Mol Cell Cardiol 37:735-45. 2004
    ..However, there are no data addressing the role of TKs in the control of single LTCC activity in human atrial cardiac myocytes, where changes in LTCC gating properties have been described in a number of disease states...
  32. ncbi request reprint Stem cell therapy: a new perspective in the treatment of patients with acute myocardial infarction
    G P Meyer
    Abt Kardiologie und Angiologie, Medizinische Hochschule, Carl Neubergstrasse 1, 30625 Hannover, Germany
    Eur J Med Res 11:439-46. 2006
    ..Ultimately, large outcome trials will have to be conducted. At the same time, continued basic research to elucidate the underlying mechanism of stem cell therapy is needed...
  33. ncbi request reprint Targeting calcineurin and associated pathways in cardiac hypertrophy and failure
    Beate Fiedler
    Hanover Medical School, Department of Cardiology and Angiology, 30625 Hanover, Germany
    Expert Opin Ther Targets 9:963-73. 2005
    ....
  34. ncbi request reprint Interference of antihypertrophic molecules and signaling pathways with the Ca2+-calcineurin-NFAT cascade in cardiac myocytes
    Beate Fiedler
    Department of Cardiology and Angiology, Hannover Medical School, Carl Neuberg Str 1, 30625, Hannover, Germany
    Cardiovasc Res 63:450-7. 2004
    ..Considering the dominant role of the calcineurin pathway in cardiac hypertrophy and failure, calcineurin-inhibitory strategies may lead to the identification of novel therapeutic approaches for patients with cardiac disease...
  35. ncbi request reprint Good manufacturing practice-compliant validation and preparation of BM cells for the therapy of acute myocardial infarction
    C Griesel
    Cytonet Hannover GmbH, Hannover, Germany
    Cytotherapy 9:35-43. 2007
    ..Thus good manufacturing practice (GMP)-compliant collection and preparation of BM for patients with AMI was established by the Cytonet group...
  36. ncbi request reprint [Pathophysiology of heart failure]
    T Kempf
    Abteilung Kardiologie und Angiologie, Medizinische Hochschule Hannover, Carl Neuberg Strasse 1, 30625, Hannover, Deutschland
    Internist (Berl) 48:899-908. 2007
    ..Thus, an increasingly complex scenario emerges with interdependent changes on the biochemical, molecular, metabolic, and cellular level. Novel therapeutic strategies may soon be based on these new pathophysiological concepts...
  37. doi request reprint Lidocaine protects from myocardial damage due to ischemia and reperfusion in mice by its antiapoptotic effects
    Dominik J Kaczmarek
    Department of Anesthesiology and Intensive Care Medicine, Hannover Medical School, Hannover, Germany
    Anesthesiology 110:1041-9. 2009
    ..Lidocaine has been demonstrated to exert antiinflammatory pleiotropic effects. The authors set out to test if lidocaine protects ischemic myocardium from reperfusion injury...
  38. ncbi request reprint Nitric oxide and the enigma of cardiac hypertrophy
    Tibor Kempf
    Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany
    Bioessays 26:608-15. 2004
    ..This delicate balance can tip towards adaptation or heart failure. In the future, patients living with cardiac disease may benefit from therapeutic strategies targeting maladaptive hypertrophy signalling pathways...
  39. ncbi request reprint Growth differentiation factor 15 for risk stratification and selection of an invasive treatment strategy in non ST-elevation acute coronary syndrome
    Kai C Wollert
    Department of Cardiology and Angiology, Hannover University Medical School, Hannover, Germany
    Circulation 116:1540-8. 2007
    ..We hypothesized that the circulating level of growth differentiation factor 15 (GDF-15) may improve risk stratification...
  40. ncbi request reprint The transforming growth factor-beta superfamily member growth-differentiation factor-15 protects the heart from ischemia/reperfusion injury
    Tibor Kempf
    Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany
    Circ Res 98:351-60. 2006
    ..In conclusion, our study identifies induction of GDF-15 in the heart as a novel defense mechanism that protects from I/R injury...
  41. ncbi request reprint Alterations in Janus kinase (JAK)-signal transducers and activators of transcription (STAT) signaling in patients with end-stage dilated cardiomyopathy
    Edith K Podewski
    Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany
    Circulation 107:798-802. 2003
    ..Little is known about the activation of this signaling pathway in the myocardia of patients with end-stage dilated cardiomyopathy (DCM)...
  42. ncbi request reprint Heme oxygenase-1 inhibition of MAP kinases, calcineurin/NFAT signaling, and hypertrophy in cardiac myocytes
    Jörn Tongers
    Department of Cardiology and Angiology, Hannover Medical School, 30625 Hannover, Germany
    Cardiovasc Res 63:545-52. 2004
    ..The inducible HO isoform, HO-1, confers protection against ischemia/reperfusion (I/R)-injury in the heart. We hypothesized that HO-1 and its catalytic by-products constitute an antihypertrophic signaling module in cardiac myocytes...
  43. ncbi request reprint Cell-based therapy for heart failure
    Kai C Wollert
    Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany
    Curr Opin Cardiol 21:234-9. 2006
    ..Experimental studies have suggested that stem cells can exert beneficial effects on the failing heart by transdifferentiating into cardiac cell types and/or by providing a source of cardioprotective paracrine factors...
  44. ncbi request reprint Growth-differentiation factor-15 improves risk stratification in ST-segment elevation myocardial infarction
    Tibor Kempf
    Department of Cardiology and Angiology, Hannover Medical School, Carl Neuberg Str 1, 30625 Hannover, Germany
    Eur Heart J 28:2858-65. 2007
    ..We explored the prognostic utility of GDF-15 in patients with ST-segment elevation myocardial infarction (STEMI) receiving fibrinolytic therapy...
  45. doi request reprint Growth differentiation factor-15 in idiopathic pulmonary arterial hypertension
    Nils Nickel
    Department of Respiratory Medicine, Hannover Medical School, Hannover, Germany
    Am J Respir Crit Care Med 178:534-41. 2008
    ..Circulating levels of GDF-15 provide independent prognostic information in patients with acute pulmonary embolism and chronic left-sided heart failure...
  46. ncbi request reprint Reduced delayed rectifier K+ current, altered electrophysiology, and increased ventricular vulnerability in MLP-deficient mice
    Ajmal Gardiwal
    Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany
    J Card Fail 13:687-93. 2007
    ..In humans, MLP-expression is downregulated both in ischemic and dilative cardiomyopathy. In this study, we investigated the effects of MLP on the electrophysiologic phenotype in vivo and on outward potassium currents...
  47. ncbi request reprint Prognostic utility of growth differentiation factor-15 in patients with chronic heart failure
    Tibor Kempf
    Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany
    J Am Coll Cardiol 50:1054-60. 2007
    ..We explored the prognostic utility of growth differentiation factor (GDF)-15 in patients with chronic heart failure (CHF)...
  48. ncbi request reprint Circulating concentrations of growth-differentiation factor 15 in apparently healthy elderly individuals and patients with chronic heart failure as assessed by a new immunoradiometric sandwich assay
    Tibor Kempf
    Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany
    Clin Chem 53:284-91. 2007
    ..There has been increasing interest in using circulating GDF15 as a biomarker in patients, for example those with cardiovascular disease...
  49. ncbi request reprint cGMP-dependent protein kinase type I inhibits TAB1-p38 mitogen-activated protein kinase apoptosis signaling in cardiac myocytes
    Beate Fiedler
    Department of Cardiology and Angiology, Hannover Medical School, Carl Neuberg Strasse 1, 30625 Hannover, Germany
    J Biol Chem 281:32831-40. 2006
    ..Together, our data identify a novel interaction between the cGMP target PKG I and the TAB1-p38 MAPK signaling pathway that serves as a defense mechanism against myocardial I/R injury...
  50. doi request reprint Conditional transgenic expression of fibroblast growth factor 9 in the adult mouse heart reduces heart failure mortality after myocardial infarction
    Mortimer Korf-Klingebiel
    Department of Cardiology and Angiology, Hannover Medical School, Carl Neuberg Strase 1, Hannover, Germany
    Circulation 123:504-14. 2011
    ..FGF9 promotes cardiac vascularization during embryonic development but is only weakly expressed in the adult heart...
  51. doi request reprint Growth differentiation factor-15: a new biomarker in cardiovascular disease
    Tibor Kempf
    Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany
    Herz 34:594-9. 2009
    ..Future studies need to evaluate prospectively whether GDF-15, alone or as part of a multimarker strategy, can improve contemporary risk prediction algorithms and support therapeutic management of patients with cardiovascular disease...
  52. doi request reprint Circulating concentrations of follistatin-like 1 in healthy individuals and patients with acute coronary syndrome as assessed by an immunoluminometric sandwich assay
    Christian Widera
    Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany
    Clin Chem 55:1794-800. 2009
    ..We hypothesized that FSTL1 can be measured in the human circulation and used as a biomarker in acute coronary syndrome (ACS)...
  53. doi request reprint Growth-differentiation factor-15 in heart failure
    Tibor Kempf
    Hannover Medical School, Hannover, Germany
    Heart Fail Clin 5:537-47. 2009
    ..A commercial assay for GDF-15 should be available in the near future...
  54. ncbi request reprint Synchronization and integration of multiple hypertrophic pathways in the heart
    Klaus Dieter Schluter
    Cardiovasc Res 63:367-72. 2004
  55. doi request reprint Growth differentiation factor-15 for prognostic assessment of patients with acute pulmonary embolism
    Mareike Lankeit
    Department of Cardiology and Pulmonology, University of Goettingen, Goettingen, Germany
    Am J Respir Crit Care Med 177:1018-25. 2008
    ..Circulating levels of GDF-15 provide independent prognostic information in patients with acute coronary syndromes or heart failure...
  56. ncbi request reprint Apoptosis repressor with caspase recruitment domain is required for cardioprotection in response to biomechanical and ischemic stress
    Stefan Donath
    Department of Cardiology, Campus Virchow Clinic, Charite, Humboldt University, HELIOS GmbH, Berlin, Germany
    Circulation 113:1203-12. 2006
    ..In this study we attempted to elucidate the physiological role of ARC and to understand pathophysiological consequences resulting from its deletion...
  57. ncbi request reprint Signal transducer and activator of transcription 3 is required for myocardial capillary growth, control of interstitial matrix deposition, and heart protection from ischemic injury
    Denise Hilfiker-Kleiner
    Department of Cardiology, Medical School Hannover, Germany
    Circ Res 95:187-95. 2004
    ....
  58. ncbi request reprint Cell therapy for acute myocardial infarction: where are we heading?
    Kai C Wollert
    Nat Clin Pract Cardiovasc Med 1:61. 2004
  59. ncbi request reprint Growth-differentiation factor-15 in cardiovascular disease: from bench to bedside, and back
    Kai C Wollert
    Basic Res Cardiol 102:412-5. 2007
  60. ncbi request reprint Carvedilol prospective randomized cumulative survival (COPERNICUS) trial: carvedilol as the sun and center of the beta-blocker world?
    Kai C Wollert
    Circulation 106:2164-6. 2002
  61. ncbi request reprint Mesenchymal stem cells for myocardial infarction: promises and pitfalls
    Kai C Wollert
    Circulation 112:151-3. 2005
  62. ncbi request reprint Growth hormone and proinflammatory cytokine activation in heart failure. Just a new verse to an old sirens' song?
    Kai C Wollert
    Eur Heart J 24:2164-5. 2003