Patrick Most

Summary

Affiliation: University of Heidelberg
Country: Germany

Publications

  1. pmc S100A1 deficiency impairs postischemic angiogenesis via compromised proangiogenic endothelial cell function and nitric oxide synthase regulation
    Patrick Most
    Center for Molecular and Translational Cardiology, Heidelberg University Hospital, 69120 Heidelberg, Germany
    Circ Res 112:66-78. 2013
  2. doi request reprint S100A1 gene therapy in small and large animals
    Patrick Most
    Department of Internal Medicine III, Center for Molecular and Translational Cardiology, University of Heidelberg, Heidelberg, Germany
    Methods Mol Biol 963:407-20. 2013
  3. ncbi request reprint Extracellular S100A1 protein inhibits apoptosis in ventricular cardiomyocytes via activation of the extracellular signal-regulated protein kinase 1/2 (ERK1/2)
    Patrick Most
    Innere Medizin III, Universitat Heidelberg, 69115 Heidelberg, Germany
    J Biol Chem 278:48404-12. 2003
  4. pmc Cardiac adenoviral S100A1 gene delivery rescues failing myocardium
    Patrick Most
    Center for Translational Medicine, Department of Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA
    J Clin Invest 114:1550-63. 2004
  5. ncbi request reprint Distinct subcellular location of the Ca2+-binding protein S100A1 differentially modulates Ca2+-cycling in ventricular rat cardiomyocytes
    Patrick Most
    Center for Translational Medicine, Department of Medicine, Thomas Jefferson University, Philadelphia, PA 19107, USA
    J Cell Sci 118:421-31. 2005
  6. ncbi request reprint S100A1 gene therapy preserves in vivo cardiac function after myocardial infarction
    Sven T Pleger
    Medizinische Universitätsklinik und Poliklinik III, Otto Meyerhof Zentrum, Universität zu Heidelberg, INF 350, 69115 Heidelberg, Germany
    Mol Ther 12:1120-9. 2005
  7. ncbi request reprint Cardiac S100A1 protein levels determine contractile performance and propensity toward heart failure after myocardial infarction
    Patrick Most
    Center for Translational Medicine, Department of Medicine, Thomas Jefferson University, Philadelphia, PA 19107, USA
    Circulation 114:1258-68. 2006
  8. ncbi request reprint Stable myocardial-specific AAV6-S100A1 gene therapy results in chronic functional heart failure rescue
    Sven T Pleger
    Center for Translational Medicine and George Zallie and Family Laboratory of Cardiovascular Gene Therapy, Thomas Jefferson University, 1025 Walnut St, Room 317, Philadelphia, PA 19107, USA
    Circulation 115:2506-15. 2007
  9. pmc AAV6.βARKct cardiac gene therapy ameliorates cardiac function and normalizes the catecholaminergic axis in a clinically relevant large animal heart failure model
    Philip W J Raake
    Department of Internal Medicine III, Cardiology, University Hospital Heidelberg, University of Heidelberg, Im Neuenheimer Feld 410, Heidelberg 69120, Germany
    Eur Heart J 34:1437-47. 2013
  10. ncbi request reprint S100A1 gene transfer: a strategy to strengthen engineered cardiac grafts
    Andrew Remppis
    Medizinische Klinik III, Universitat Heidelberg, 69115 Heidelberg, Germany
    J Gene Med 6:387-94. 2004

Collaborators

Detail Information

Publications34

  1. pmc S100A1 deficiency impairs postischemic angiogenesis via compromised proangiogenic endothelial cell function and nitric oxide synthase regulation
    Patrick Most
    Center for Molecular and Translational Cardiology, Heidelberg University Hospital, 69120 Heidelberg, Germany
    Circ Res 112:66-78. 2013
    ..Mice lacking the EF-hand Ca2+ sensor S100A1 display endothelial dysfunction because of distorted Ca2+ -activated nitric oxide (NO) generation...
  2. doi request reprint S100A1 gene therapy in small and large animals
    Patrick Most
    Department of Internal Medicine III, Center for Molecular and Translational Cardiology, University of Heidelberg, Heidelberg, Germany
    Methods Mol Biol 963:407-20. 2013
    ..Here we describe myocardial gene therapy in small and large animal models of postischemic heart failure used to reveal the positive inotrope, antihypertrophic, and pro-energetic action of the small calcium sensor protein S100A1...
  3. ncbi request reprint Extracellular S100A1 protein inhibits apoptosis in ventricular cardiomyocytes via activation of the extracellular signal-regulated protein kinase 1/2 (ERK1/2)
    Patrick Most
    Innere Medizin III, Universitat Heidelberg, 69115 Heidelberg, Germany
    J Biol Chem 278:48404-12. 2003
    ..These findings warrant speculation that injury-dependent release of the S100A1 protein from cardiomyocytes may serve as an intrinsic mechanism to promote survival of the myocardium in vivo...
  4. pmc Cardiac adenoviral S100A1 gene delivery rescues failing myocardium
    Patrick Most
    Center for Translational Medicine, Department of Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA
    J Clin Invest 114:1550-63. 2004
    ..Thus, the present study demonstrates that restoration of S100A1 protein levels in failing myocardium by gene transfer may be a novel therapeutic strategy for the treatment of heart failure...
  5. ncbi request reprint Distinct subcellular location of the Ca2+-binding protein S100A1 differentially modulates Ca2+-cycling in ventricular rat cardiomyocytes
    Patrick Most
    Center for Translational Medicine, Department of Medicine, Thomas Jefferson University, Philadelphia, PA 19107, USA
    J Cell Sci 118:421-31. 2005
    ..This study provides the first evidence that intracellular S100A1, depending on its subcellular location, modulates cardiac Ca2+-turnover via different Ca2+-regulatory proteins...
  6. ncbi request reprint S100A1 gene therapy preserves in vivo cardiac function after myocardial infarction
    Sven T Pleger
    Medizinische Universitätsklinik und Poliklinik III, Otto Meyerhof Zentrum, Universität zu Heidelberg, INF 350, 69115 Heidelberg, Germany
    Mol Ther 12:1120-9. 2005
    ..Also, S100A1 overexpression reduced cardiac hypertrophy 1 week post-MI. Overall, our data indicate that S100A1 gene therapy provides a potential novel treatment strategy to maintain contractile performance of the post-MI heart...
  7. ncbi request reprint Cardiac S100A1 protein levels determine contractile performance and propensity toward heart failure after myocardial infarction
    Patrick Most
    Center for Translational Medicine, Department of Medicine, Thomas Jefferson University, Philadelphia, PA 19107, USA
    Circulation 114:1258-68. 2006
    ....
  8. ncbi request reprint Stable myocardial-specific AAV6-S100A1 gene therapy results in chronic functional heart failure rescue
    Sven T Pleger
    Center for Translational Medicine and George Zallie and Family Laboratory of Cardiovascular Gene Therapy, Thomas Jefferson University, 1025 Walnut St, Room 317, Philadelphia, PA 19107, USA
    Circulation 115:2506-15. 2007
    ..An attractive approach is gene therapy; however, the clinical barrier has yet to be broken because of several issues, including the lack of an ideal vector supporting safe and long-term myocardial transgene expression...
  9. pmc AAV6.βARKct cardiac gene therapy ameliorates cardiac function and normalizes the catecholaminergic axis in a clinically relevant large animal heart failure model
    Philip W J Raake
    Department of Internal Medicine III, Cardiology, University Hospital Heidelberg, University of Heidelberg, Im Neuenheimer Feld 410, Heidelberg 69120, Germany
    Eur Heart J 34:1437-47. 2013
    ..This study was designed to evaluate long-term βARKct expression in a clinically relevant large animal HF model, using stable myocardial gene delivery with adeno-associated virus serotype 6 (AAV6)...
  10. ncbi request reprint S100A1 gene transfer: a strategy to strengthen engineered cardiac grafts
    Andrew Remppis
    Medizinische Klinik III, Universitat Heidelberg, 69115 Heidelberg, Germany
    J Gene Med 6:387-94. 2004
    ..Here, we explore a strategy to improve contractile properties of engineered heart tissue (EHT) by S100A1 gene transfer...
  11. ncbi request reprint Cardiac AAV9-S100A1 gene therapy rescues post-ischemic heart failure in a preclinical large animal model
    Sven T Pleger
    Center for Molecular and Translational Cardiology, University of Heidelberg, 69120 Heidelberg, Germany
    Sci Transl Med 3:92ra64. 2011
    ..Our results present a strong rationale for a clinical trial of S100A1 gene therapy for human heart failure that could potentially complement current strategies to treat end-stage heart failure...
  12. pmc G protein-coupled receptor kinase 2 ablation in cardiac myocytes before or after myocardial infarction prevents heart failure
    Philip W Raake
    Center for Translational Medicine, Department of Medicine, Thomas Jefferson University, 1025 Walnut St, Philadelphia, PA 19107, USA
    Circ Res 103:413-22. 2008
    ....
  13. doi request reprint Endothelial S100A1 modulates vascular function via nitric oxide
    Sven T Pleger
    Center for Translational Medicine, Thomas Jefferson University, Philadelphia, PA 19107, USA
    Circ Res 102:786-94. 2008
    ..Targeting endothelial S100A1 expression may, therefore, be a novel therapeutic means to improve endothelial function in vascular disease or heart failure...
  14. ncbi request reprint Targeting myocardial beta-adrenergic receptor signaling and calcium cycling for heart failure gene therapy
    Sven T Pleger
    George Zallie and Family Laboratory for Cardiovascular Gene Therapy, Center for Translational Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA
    J Card Fail 13:401-14. 2007
    ....
  15. ncbi request reprint S100A1 decreases calcium spark frequency and alters their spatial characteristics in permeabilized adult ventricular cardiomyocytes
    Mirko Völkers
    Department of Internal Medicine III, Laboratory for Cardiac Stem Cell and Gene Therapy, Division of Cardiology, INF 350, University of Heidelberg, 69120 Heidelberg, Germany
    Cell Calcium 41:135-43. 2007
    ..6) remained unaltered by S100A1. Hence, we propose S100A1 as a novel inhibitory modulator of RyR2 function at diastolic Ca2+-concentrations in rabbit ventricular cardiomyocytes...
  16. pmc BMP-2 and FGF-2 synergistically facilitate adoption of a cardiac phenotype in somatic bone marrow c-kit+/Sca-1+ stem cells
    Brent R DeGeorge
    Center for Translational Medicine, Department of Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania, USA
    Clin Transl Sci 1:116-25. 2008
    ....
  17. doi request reprint Heart failure gene therapy: the path to clinical practice
    Sven T Pleger
    Center for Molecular and Translational Cardiology, Department of Internal Medicine III, Germany
    Circ Res 113:792-809. 2013
    ..The objective of this review is to discuss the current state of the art in the field and point out inevitable innovations on which the future evolution of heart failure gene therapy into an effective and safe clinical treatment relies. ..
  18. pmc The inotropic peptide βARKct improves βAR responsiveness in normal and failing cardiomyocytes through G(βγ)-mediated L-type calcium current disinhibition
    Mirko Völkers
    Center for Molecular and Translational Cardiology, University of Heidelberg, Germany
    Circ Res 108:27-39. 2011
    ..However, molecular targets mediating improved cardiac contractile performance by βARKct and its impact on G(βγ)-mediated signaling have yet to be fully elucidated...
  19. pmc S100A1: a multifaceted therapeutic target in cardiovascular disease
    David Rohde
    Laboratory for Molecular and Translational Cardiology, Division of Cardiology, Department of Internal Medicine III, University of Heidelberg, INF 350, 69120 Heidelberg, Germany
    J Cardiovasc Transl Res 3:525-37. 2010
    ..In summary, elaborate basic and translational research established S100A1 as a multifaceted therapeutic target in cardiovascular disease, providing a promising novel therapeutic strategy to future cardiologists...
  20. doi request reprint Orai1 and Stim1 regulate normal and hypertrophic growth in cardiomyocytes
    Mirko Voelkers
    Department of Internal Medicine III, Laboratory for Molecular and Translational Cardiology, Division of Cardiology, INF 350, University of Heidelberg, 69120 Heidelberg, Germany
    J Mol Cell Cardiol 48:1329-34. 2010
    ..This study shows for the first time that both Orai1 and Stim1 have a key role in cardiomyocyte SOCE regulating both normal and hypertrophic postnatal cardiac growth in vitro...
  21. ncbi request reprint S100A1: a novel inotropic regulator of cardiac performance. Transition from molecular physiology to pathophysiological relevance
    Patrick Most
    Center for Translational Medicine, Laboratory for Cardiac Stem Cell and Gene Therapy, Department of Medicine, Thomas Jefferson University, Philadelphia, PA 19107, USA
    Am J Physiol Regul Integr Comp Physiol 293:R568-77. 2007
    ..Subsequently, therapeutic options by means of genetic manipulation of cardiac S100A1 expression will be discussed, aiming to complete our current understanding of the role of S100A1 in diseased myocardium...
  22. ncbi request reprint Hope for a broken heart?
    Patrick Most
    Division of Cardiology, Department of Internal Medicine III, University of Heidelberg, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany
    Trends Biotechnol 22:487-9. 2004
    ..This proof-of-concept study has great importance for future heart failure therapy because it provides evidence for the therapeutic effectiveness of betaARK1 inhibition in failing human myocardium...
  23. pmc S100A1 in cardiovascular health and disease: closing the gap between basic science and clinical therapy
    Carolin Kraus
    Center for Translational Medicine, Laboratory for Cardiac Stem Cell and Gene Therapy Department of Medicine, Thomas Jefferson University, Philadelphia, PA 19107, USA
    J Mol Cell Cardiol 47:445-55. 2009
    ....
  24. pmc Cardiac G-protein-coupled receptor kinase 2 ablation induces a novel Ca2+ handling phenotype resistant to adverse alterations and remodeling after myocardial infarction
    Philip W Raake
    Department of Internal Medicine III, Cardiology, University of Heidelberg, Germany
    Circulation 125:2108-18. 2012
    ..G-protein-coupled receptor kinase 2 ablation impedes heart failure development, but elucidation of the cellular mechanisms has not been achieved, and such elucidation is the aim of this study...
  25. pmc S100A1: a regulator of striated muscle sarcoplasmic reticulum Ca2+ handling, sarcomeric, and mitochondrial function
    Mirko Völkers
    Division of Cardiology, Department of Internal Medicine III, Laboratory for Molecular and Translational Cardiology, University of Heidelberg, INF 350, 69120 Heidelberg, Germany
    J Biomed Biotechnol 2010:178614. 2010
    ....
  26. pmc Level of G protein-coupled receptor kinase-2 determines myocardial ischemia/reperfusion injury via pro- and anti-apoptotic mechanisms
    Henriette Brinks
    George Zallie and Family Laboratory for Cardiovascular Gene Therapy, Center for Translational Medicine, Jefferson Medical College, Thomas Jefferson University, 1025 Walnut Street, Philadelphia, PA 19107, USA
    Circ Res 107:1140-9. 2010
    ..GPCR signaling pathways are regulated by GPCR kinases (GRKs), and GRK2 has been shown to be a critical molecule in normal and pathological cardiac function...
  27. pmc Simultaneous administration of insulin-like growth factor-1 and darbepoetin alfa protects the rat myocardium against myocardial infarction and enhances angiogenesis
    Matthieu Boucher
    George Zallie and Family Laboratory for Cardiovascular Gene Therapy, Center for Translational Medicine, Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania, USA
    Clin Transl Sci 1:13-20. 2008
    ..This protection results in reduced infarct size and improved cardiac function. Moreover, this treatment reduces apoptosis and enhances angiogenesis in the ischemic heart...
  28. pmc Increased proinflammatory endothelial response to S100A8/A9 after preactivation through advanced glycation end products
    Philipp Ehlermann
    Universitat Heidelberg, Abteilung Innere Medizin III, Heidelberg, Germany
    Cardiovasc Diabetol 5:6. 2006
    ..As recently S100 proteins have been identified as ligands of RAGE, we sought to determine the effects of the proinflammatory heterodimer of S100A8/S100A9 on the RAGE-NFkappaB mediated induction of proinflammatory gene expression...
  29. ncbi request reprint The C terminus (amino acids 75-94) and the linker region (amino acids 42-54) of the Ca2+-binding protein S100A1 differentially enhance sarcoplasmic Ca2+ release in murine skinned skeletal muscle fibers
    Patrick Most
    Abteilung Innere Medizin III Kardiologie, Universitat Heidelberg, 69115 Heidelberg, Germany
    J Biol Chem 278:26356-64. 2003
    ..Thus, our data suggest that S100A1 may serve as an endogenous enhancer of SR Ca2+ release and might therefore be of physiological relevance in the process of excitation-contraction coupling in skeletal muscle...
  30. doi request reprint S100A1 gene therapy for heart failure: a novel strategy on the verge of clinical trials
    David Rohde
    Laboratory for Molecular and Translational Cardiology, Center for Molecular and Translational Cardiology, Department of Internal Medicine III, University of Heidelberg, Heidelberg, Germany
    J Mol Cell Cardiol 50:777-84. 2011
    ..This article is part of a Special Section entitled "Special Section: Cardiovascular Gene Therapy"...
  31. ncbi request reprint S100A1 is released from ischemic cardiomyocytes and signals myocardial damage via Toll-like receptor 4
    David Rohde
    Section of Molecular and Translational Cardiology, Department of Internal Medicine III, Heidelberg University Hospital Heidelberg University, Heidelberg, Germany
    EMBO Mol Med 6:778-94. 2014
    ..Our study demonstrates alarmin properties for S100A1 from necrotic cardiomyocytes. However, the potentially beneficial role of extracellular S100A1 in MI-related inflammation and repair warrants further investigation. ..
  32. pmc VEGF-PLCgamma1 pathway controls cardiac contractility in the embryonic heart
    Wolfgang Rottbauer
    Department of Medicine III, University of Heidelberg, D 69120 Heidelberg, Germany
    Genes Dev 19:1624-34. 2005
    ..Thus, the muscle of the heart uses the VEGF-PLCgamma1 cascade to control the strength of the heart beat. We speculate that this paracrine system may contribute to normal and pathological regulation of cardiac contractility...
  33. doi request reprint Decreased contractility due to energy deprivation in a transgenic rat model of hypertrophic cardiomyopathy
    Mark Luedde
    Department of Cardiology, University of Heidelberg, Germany
    J Mol Med (Berl) 87:411-22. 2009
    ..In summary, we demonstrate profound energetic alterations in DEL-TNT hearts, supporting the notion that inefficient cellular ATP utilization contributes to the pathogenesis of HCM...
  34. pmc Long-term survival of cancer patients compared to heart failure and stroke: a systematic review
    Vasileios Askoxylakis
    Department of Radiooncology and Radiation Therapy, University of Heidelberg, Im Neuenheimer Feld 400, 69120, Heidelberg, Germany
    BMC Cancer 10:105. 2010
    ..Aim of this study is to provide an overview of long term survival of cancer, heart failure and stroke patients based on the results of large population- and hospital-based studies...