Georg Schett

Summary

Affiliation: University of Vienna
Country: Austria

Publications

  1. ncbi [Reciprocal modification of Fas activation and stress protein response decides apoptosis or resistance development of cells]
    G Schett
    Abteilung Rheumatologie der Universitätsklinik für Innere Medizin III, Wien
    Acta Med Austriaca 27:94-8. 2000
  2. ncbi Osteoprotegerin protects against generalized bone loss in tumor necrosis factor-transgenic mice
    Georg Schett
    Department of Internal Medicine III, Division of Rheumatology, University of Vienna, Wahringer Gurtel 18 20, A 1090 Vienna, Austria
    Arthritis Rheum 48:2042-51. 2003
  3. ncbi TNFalpha mediates susceptibility to heat-induced apoptosis by protein phosphatase-mediated inhibition of the HSF1/hsp70 stress response
    G Schett
    Division of Rheumatology, Department of Internal Medicine III, University of Vienna, Austria
    Cell Death Differ 10:1126-36. 2003
  4. ncbi Single and combined inhibition of tumor necrosis factor, interleukin-1, and RANKL pathways in tumor necrosis factor-induced arthritis: effects on synovial inflammation, bone erosion, and cartilage destruction
    Jochen Zwerina
    University of Vienna, Vienna, Austria
    Arthritis Rheum 50:277-90. 2004
  5. ncbi Obstruction of the pulmonary artery by granulomatous vasculitis: a clinical, morphological, and immunological analysis
    G Schett
    Division of Rheumatology, Department of Internal Medicine III, University of Vienna, Austria
    Ann Rheum Dis 61:463-7. 2002
  6. ncbi Soluble RANKL and risk of nontraumatic fracture
    Georg Schett
    Department of Internal Medicine III, Division of Rheumatology, University of Vienna, Vienna, Austria
    JAMA 291:1108-13. 2004
  7. ncbi Adenovirus-based overexpression of tissue inhibitor of metalloproteinases 1 reduces tissue damage in the joints of tumor necrosis factor alpha transgenic mice
    G Schett
    Department of Internal Medicine III, University of Vienna, Austria
    Arthritis Rheum 44:2888-98. 2001
  8. ncbi Serum leptin level and the risk of nontraumatic fracture
    Georg Schett
    Division of Rheumatology, Department of Internal Medicine III, University of Vienna, Austria
    Am J Med 117:952-6. 2004
  9. ncbi The stressed synovium
    G Schett
    Department of Internal Medicine III, University of Vienna, Wahringer Gurtel 18 20, A 1180 Vienna, Austria
    Arthritis Res 3:80-6. 2001
  10. ncbi The role of osteoprotegerin in arthritis
    Georg Schett
    Department of Internal Medicine III, Division of Rheumatology, University of Vienna, Austria
    Arthritis Res Ther 5:239-45. 2003

Detail Information

Publications74

  1. ncbi [Reciprocal modification of Fas activation and stress protein response decides apoptosis or resistance development of cells]
    G Schett
    Abteilung Rheumatologie der Universitätsklinik für Innere Medizin III, Wien
    Acta Med Austriaca 27:94-8. 2000
    ..Thus, we conclude that inhibition of the HSF1/hsp70 stress response during Fas-mediated apoptosis and vice versa may facilitate a cell to pass a previously chosen pathway, stress resistance or apoptosis...
  2. ncbi Osteoprotegerin protects against generalized bone loss in tumor necrosis factor-transgenic mice
    Georg Schett
    Department of Internal Medicine III, Division of Rheumatology, University of Vienna, Wahringer Gurtel 18 20, A 1090 Vienna, Austria
    Arthritis Rheum 48:2042-51. 2003
    ..To investigate the role of tumor necrosis factor (TNF) in systemic bone loss of chronic inflammatory conditions, such as rheumatoid arthritis (RA), and to address the therapeutic potential of osteoclast blockade...
  3. ncbi TNFalpha mediates susceptibility to heat-induced apoptosis by protein phosphatase-mediated inhibition of the HSF1/hsp70 stress response
    G Schett
    Division of Rheumatology, Department of Internal Medicine III, University of Vienna, Austria
    Cell Death Differ 10:1126-36. 2003
    ..The price of inhibition of an essential cellular stress response is increased sensitivity to apoptotic cell death...
  4. ncbi Single and combined inhibition of tumor necrosis factor, interleukin-1, and RANKL pathways in tumor necrosis factor-induced arthritis: effects on synovial inflammation, bone erosion, and cartilage destruction
    Jochen Zwerina
    University of Vienna, Vienna, Austria
    Arthritis Rheum 50:277-90. 2004
    ..To investigate the efficacy of single and combined blockade of tumor necrosis factor (TNF), interleukin-1 (IL-1), and RANKL pathways on synovial inflammation, bone erosion, and cartilage destruction in a TNF-driven arthritis model...
  5. ncbi Obstruction of the pulmonary artery by granulomatous vasculitis: a clinical, morphological, and immunological analysis
    G Schett
    Division of Rheumatology, Department of Internal Medicine III, University of Vienna, Austria
    Ann Rheum Dis 61:463-7. 2002
  6. ncbi Soluble RANKL and risk of nontraumatic fracture
    Georg Schett
    Department of Internal Medicine III, Division of Rheumatology, University of Vienna, Vienna, Austria
    JAMA 291:1108-13. 2004
    ..The receptor activator of nuclear factor kappaB ligand (RANKL) is essential for osteoclast and, possibly, osteoblast activation and may represent a key link between bone formation and resorption...
  7. ncbi Adenovirus-based overexpression of tissue inhibitor of metalloproteinases 1 reduces tissue damage in the joints of tumor necrosis factor alpha transgenic mice
    G Schett
    Department of Internal Medicine III, University of Vienna, Austria
    Arthritis Rheum 44:2888-98. 2001
    ....
  8. ncbi Serum leptin level and the risk of nontraumatic fracture
    Georg Schett
    Division of Rheumatology, Department of Internal Medicine III, University of Vienna, Austria
    Am J Med 117:952-6. 2004
  9. ncbi The stressed synovium
    G Schett
    Department of Internal Medicine III, University of Vienna, Wahringer Gurtel 18 20, A 1180 Vienna, Austria
    Arthritis Res 3:80-6. 2001
    ..Stress signalling pathways are therefore new and promising targets of future anti-rheumatic therapies...
  10. ncbi The role of osteoprotegerin in arthritis
    Georg Schett
    Department of Internal Medicine III, Division of Rheumatology, University of Vienna, Austria
    Arthritis Res Ther 5:239-45. 2003
    ..In addition, the role of OPG as a therapeutic tool to inhibit local bone erosion is addressed. Finally, evidence for OPG as an inhibitor of systemic inflammatory bone loss is discussed...
  11. ncbi Tumour necrosis factor activates the mitogen-activated protein kinases p38alpha and ERK in the synovial membrane in vivo
    Birgit Görtz
    Division of Rheumatology, Department of Internal Medicine III, University of Vienna, Vienna, Austria
    Arthritis Res Ther 7:R1140-7. 2005
    ....
  12. ncbi Tenosynovitis and osteoclast formation as the initial preclinical changes in a murine model of inflammatory arthritis
    Silvia Hayer
    Medical University of Vienna, Vienna, Austria
    Arthritis Rheum 56:79-88. 2007
    ..To determine the nature of the initial changes of joint inflammation occurring before, at the time of, and shortly after onset of clinically apparent arthritis...
  13. ncbi JNK1 is not essential for TNF-mediated joint disease
    Marcus Koller
    Department of Internal Medicine III, Division of Rheumatology, Medical University of Vienna, Austria
    Arthritis Res Ther 7:R166-73. 2005
    ..Thus, JNK1 activation does not seem to be essential for TNF-mediated arthritis...
  14. ncbi Heme oxygenase 1 (HO-1) regulates osteoclastogenesis and bone resorption
    Jochen Zwerina
    Division of Rheumatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria
    FASEB J 19:2011-3. 2005
    ..In summary, these data indicate that HO-1 negatively regulates osteoclastogenesis, leading to a positive net balance of bone...
  15. ncbi Zoledronic acid protects against local and systemic bone loss in tumor necrosis factor-mediated arthritis
    Petra Herrak
    University of Vienna, Vienna, Austria
    Arthritis Rheum 50:2327-37. 2004
    ..In addition to their role in antiinflammatory drug therapy, modern bisphosphonates are promising candidates for maintaining joint integrity and reversing systemic bone loss in patients with arthritis...
  16. ncbi Activation of p38 MAPK is a key step in tumor necrosis factor-mediated inflammatory bone destruction
    Jochen Zwerina
    Medical University of Vienna, Vienna, Austria
    Arthritis Rheum 54:463-72. 2006
    ....
  17. ncbi Repair of local bone erosions and reversal of systemic bone loss upon therapy with anti-tumor necrosis factor in combination with osteoprotegerin or parathyroid hormone in tumor necrosis factor-mediated arthritis
    Kurt Redlich
    Department of Internal Medicine III, University of Vienna, Vienna, Austria
    Am J Pathol 164:543-55. 2004
    ....
  18. ncbi Tumor necrosis factor alpha-mediated joint destruction is inhibited by targeting osteoclasts with osteoprotegerin
    Kurt Redlich
    University of Vienna, Vienna, Austria
    Arthritis Rheum 46:785-92. 2002
    ....
  19. ncbi Additive bone-protective effects of anabolic treatment when used in conjunction with RANKL and tumor necrosis factor inhibition in two rat arthritis models
    Georg Schett
    Amgen Inc, Thousand Oaks, California, and Medical University of Vienna, Vienna, Austria
    Arthritis Rheum 52:1604-11. 2005
    ..CONCLUSION: The bone-protective effects resulting from RANKL or TNF antagonism can be further improved by the addition of a bone anabolic agent...
  20. ncbi PI3Kgamma regulates cartilage damage in chronic inflammatory arthritis
    Silvia Hayer
    Division of Rheumatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria
    FASEB J 23:4288-98. 2009
    ....
  21. ncbi Antiinflammatory effects of tumor necrosis factor on hematopoietic cells in a murine model of erosive arthritis
    Stephan Blüml
    Medical University of Vienna and Center of Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria
    Arthritis Rheum 62:1608-19. 2010
    ....
  22. ncbi The rheumatoid arthritis-associated autoantigen hnRNP-A2 (RA33) is a major stimulator of autoimmunity in rats with pristane-induced arthritis
    Markus H Hoffmann
    Department of Rheumatology, Medical University of Vienna, Vienna, Austria
    J Immunol 179:7568-76. 2007
    ..Taken together, these data suggest hnRNP-A2 to be among the primary inducers of autoimmunity in PIA. Therefore, this Ag might play a pivotal role in the pathogenesis of PIA and possibly also human RA...
  23. ncbi Differentially regulated expression of growth differentiation factor 5 and bone morphogenetic protein 7 in articular cartilage and synovium in murine chronic arthritis: potential importance for cartilage breakdown and synovial hypertrophy
    Klaus Bobacz
    University of Vienna, Vienna, Austria
    Arthritis Rheum 58:109-18. 2008
    ....
  24. ncbi Osteoclasts are essential for TNF-alpha-mediated joint destruction
    Kurt Redlich
    Department of Internal Medicine III, Division of Rheumatology, University of Vienna, Vienna, Austria
    J Clin Invest 110:1419-27. 2002
    ..Therefore, in addition to the use of anti-inflammatory therapies, osteoclast inhibition could be beneficial for the treatment of rheumatoid arthritis...
  25. ncbi CD44 is a determinant of inflammatory bone loss
    Silvia Hayer
    Division of Rheumatology, Department of Internal Medicine III, Medical University of Vienna, A 1090 Vienna, Austria
    J Exp Med 201:903-14. 2005
    ..These data identify CD44 as a critical inhibitor of TNF-driven joint destruction and inflammatory bone loss...
  26. ncbi Aberrant expression of the autoantigen heterogeneous nuclear ribonucleoprotein-A2 (RA33) and spontaneous formation of rheumatoid arthritis-associated anti-RA33 autoantibodies in TNF-alpha transgenic mice
    Silvia Hayer
    Department of Rheumatology, Internal Medicine III, Medical University of Vienna, Vienna, Austria
    J Immunol 175:8327-36. 2005
    ..These findings suggest that overproduction of TNF-alpha leads to aberrant expression of hnRNP-A2 in the rheumatoid joint and subsequently to autoimmune reactions, which may enhance the inflammatory and destructive process...
  27. ncbi Imbalance of local bone metabolism in inflammatory arthritis and its reversal upon tumor necrosis factor blockade: direct analysis of bone turnover in murine arthritis
    Jochen Zwerina
    Division of Rheumatology, Department of Internal Medicine III, Medical University of Vienna, Waehringer Guertel 18 20, A 1090 Vienna, Austria
    Arthritis Res Ther 8:R22. 2006
    ..These data indicate that bone resorption dominates at skeletal sites close to synovial inflammatory tissue, whereas bone formation is induced at more distant sites attempting to counter-regulate bone resorption...
  28. ncbi Mammalian target of rapamycin signaling is crucial for joint destruction in experimental arthritis and is activated in osteoclasts from patients with rheumatoid arthritis
    Daniel Cejka
    Medical University of Vienna, Vienna, Austria
    Arthritis Rheum 62:2294-302. 2010
    ..To date, the contribution of mTOR signaling to joint inflammation and structural bone and cartilage damage is unknown. The aim of this study was to investigate the potential of inhibiting mTOR as a treatment of inflammatory arthritis...
  29. ncbi Rheumatoid arthritis: inflammation and bone loss
    Georg Schett
    Division of Rheumatology, Department of Internal Medicine III, University of Vienna, Vienna, Austria
    Wien Med Wochenschr 156:34-41. 2006
    ..This review describes the mechanism of inflammatory bone loss, describes its cellular and molecular players and gives insights in current therapeutic tools to inhibit this process...
  30. ncbi Interaction between synovial inflammatory tissue and bone marrow in rheumatoid arthritis
    Esther Jimenez-Boj
    Division of Rheumatology, Department of Internal Medicine III, Medical University of Vienna, Austria
    J Immunol 175:2579-88. 2005
    ..This suggests that bone marrow is an additional compartment in the disease process of RA...
  31. ncbi B-cell infiltrates induce endosteal bone formation in inflammatory arthritis
    Silvia Hayer
    Division of Rheumatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria
    J Bone Miner Res 23:1650-60. 2008
    ....
  32. ncbi Pathogenesis of rheumatoid arthritis: targeting cytokines
    Jochen Zwerina
    Division of Rheumatology, Internal Medicine III, Medical University of Vienna, Waehringer Guertel 18-20, A-1090 Vienna, Austria
    Ann N Y Acad Sci 1051:716-29. 2005
    ....
  33. ncbi Rheumatoid arthritis therapy after tumor necrosis factor and interleukin-1 blockade
    Kurt Redlich
    University of Vienna, Vienna, Austria
    Arthritis Rheum 48:3308-19. 2003
  34. ncbi Differential tissue expression and activation of p38 MAPK alpha, beta, gamma, and delta isoforms in rheumatoid arthritis
    Adelheid Korb
    Medical University of Vienna, Vienna, Austria
    Arthritis Rheum 54:2745-56. 2006
    ..CONCLUSION: These data show that the alpha and gamma isoforms of p38 MAPK dominate in chronic inflammation. Effective strategies to inhibit p38 MAPK should therefore aim to specifically target either or both of these isoforms...
  35. ncbi Pro-inflammatory cytokines in rheumatoid arthritis: pathogenetic and therapeutic aspects
    Josef S Smolen
    Division of Rheumatology, Internal Medicine III, Medical University of Vienna, Austria
    Clin Rev Allergy Immunol 28:239-48. 2005
    ....
  36. ncbi TNF-induced structural joint damage is mediated by IL-1
    Jochen Zwerina
    Department of Internal Medicine III, Medical University of Vienna, A 1090 Vienna, Austria
    Proc Natl Acad Sci U S A 104:11742-7. 2007
    ..These data show that TNF-mediated cartilage damage is completely and TNF-mediated bone damage is partially dependent on IL-1, suggesting that IL-1 is a crucial mediator for inflammatory cartilage and bone degradation...
  37. ncbi New insights in the mechanism of bone loss in arthritis
    Georg Schett
    Division of Rheumatology, Department of Internal Medicine III, University of Vienna, Vienna, Austria
    Curr Pharm Des 11:3039-49. 2005
    ..In contrast, chronic forms of arthritis, such as psoriatic arthritis or rheumatoid arthritis (RA) are usually destructive and lead to alteration of joint structure and functional impairment...
  38. ncbi Arthritis -- a nightmare for bone
    Georg Schett
    Department of Internal Medicine III, Division of Rheumatology, Medical University of Vienna, Vienna, Austria
    Wien Klin Wochenschr 118:11-5. 2006
  39. ncbi Listeria-associated arthritis in a patient undergoing etanercept therapy: case report and review of the literature
    Georg Schett
    Division of Rheumatology, Department of Internal Medicine III, University of Vienna, Wahringer Gurtel 18 20, A 1090 Vienna, Austria
    J Clin Microbiol 43:2537-41. 2005
    ..We review the literature of articular listeriosis and discuss the role of tumor necrosis factor blockade in precipitating listeriosis...
  40. ncbi Bone erosions and bone marrow edema as defined by magnetic resonance imaging reflect true bone marrow inflammation in rheumatoid arthritis
    Esther Jimenez Boj
    Medical University of Vienna, Vienna, Austria
    Arthritis Rheum 56:1118-24. 2007
    ..To investigate the pathologic nature of features termed "bone erosion" and "bone marrow edema" (also called "osteitis) on magnetic resonance imaging (MRI) scans of joints affected by rheumatoid arthritis (RA)...
  41. ncbi Overexpression of transcription factor Ets-1 in rheumatoid arthritis synovial membrane: regulation of expression and activation by interleukin-1 and tumor necrosis factor alpha
    K Redlich
    University of Vienna, Austria
    Arthritis Rheum 44:266-74. 2001
    ....
  42. ncbi Quantitative ultrasound in the assessment of bone status of patients suffering from rheumatic diseases
    I Lernbass
    Department of Pathophysiology, University of Vienna, Vienna, Austria
    Skeletal Radiol 31:270-6. 2002
    ..To explore the effects of rheumatic diseases and glucocorticoids on bone mass a group of patients suffering from systemic lupus erythematosus (SLE, n=18) and rheumatoid arthritis (RA, n=22) were examined...
  43. ncbi B cell epitopes of the heterogeneous nuclear ribonucleoprotein A2: identification of a new specific antibody marker for active lupus disease
    G Schett
    Division of Rheumatology, Internal Medicine III, Medical University of Vienna, Austria
    Ann Rheum Dis 68:729-35. 2009
    ....
  44. ncbi Decreased serum erythropoietin and its relation to anti-erythropoietin antibodies in anaemia of systemic lupus erythematosus
    G Schett
    Division of Rheumatology, Department of Internal Medicine III, University of Vienna Medical School, Vienna, Austria
    Rheumatology (Oxford) 40:424-31. 2001
    ..Anti-erythropoietin antibodies are frequently present in SLE and interfere with the measurement of serum erythropoietin level. However, these antibodies are not associated with increased severity of SLE-associated anaemia...
  45. ncbi Inflammation and destruction of the joints--the Wnt pathway
    K Polzer
    Joint Bone Spine 75:105-7. 2008
  46. ncbi Treg cells suppress osteoclast formation: a new link between the immune system and bone
    Mario M Zaiss
    Department of Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen Nuremberg, Krankenhausstrasse 12, Erlangen, Germany
    Arthritis Rheum 56:4104-12. 2007
    ..To investigate whether Treg cells can suppress osteoclast differentiation, and to define a new potential link between the immune system and the skeleton...
  47. ncbi Review: Immune cells and mediators of inflammatory arthritis
    Georg Schett
    Department of Internal Medicine 3, University of Erlangen Nurnberg, Erlangen, Germany
    Autoimmunity 41:224-9. 2008
    ..Inhibition of osteoclast formation has proven as an effective approach to inhibit structural damage in experimental arthritis and preliminary data suggest that such approaches are also effective in human RA...
  48. ncbi Overexpression of tumor necrosis factor causes bilateral sacroiliitis
    Kurt Redlich
    University of Vienna Vienna, Austria
    Arthritis Rheum 50:1001-5. 2004
  49. ncbi Joint remodelling in inflammatory disease
    Georg Schett
    Department of Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen Nuremberg, Krankenhausstrasse 12, D 91054 Erlangen, Germany
    Ann Rheum Dis 66:iii42-4. 2007
    ..Whereas a short and self-limited activation of the immune system has no clinically meaningful effect on bone, prolonged immune activation as found in chronic inflammatory disease inevitably leads to bone wasting...
  50. ncbi Osteoprotegerin is a risk factor for progressive atherosclerosis and cardiovascular disease
    Stefan Kiechl
    Department of Neurology, University Clinic, Anichstrasse 35, A 6020 Innsbruck, Austria
    Circulation 109:2175-80. 2004
    ..Recent experimental research has implicated osteoprotegerin in atherogenesis, but epidemiological confirmation of this concept is sparse...
  51. ncbi Cathepsin K deficiency partially inhibits, but does not prevent, bone destruction in human tumor necrosis factor-transgenic mice
    Uta Schurigt
    Friedrich Schiller University, Jena, Germany
    Arthritis Rheum 58:422-34. 2008
    ....
  52. ncbi The lonely death: chondrocyte apoptosis in TNF-induced arthritis
    Karin Polzer
    Department of Internal Medicine 3, Institute of Clinical Immunology, University of Erlangen, Erlangen, Germany
    Autoimmunity 40:333-6. 2007
    ..These data indicate that chondrocyte death may play a primary role in inflammatory arthritis fueling cartilage inflammation and damage due to secondary necrosis...
  53. ncbi Tumour necrosis factor blockers and structural remodelling in ankylosing spondylitis: what is reality and what is fiction?
    Georg Schett
    Ann Rheum Dis 66:709-11. 2007
  54. ncbi Mechanisms of Disease: the link between RANKL and arthritic bone disease
    Georg Schett
    Medical University of Vienna, Austria
    Nat Clin Pract Rheumatol 1:47-54. 2005
    ..Therefore, inhibition of RANKL is regarded as a promising future strategy for inhibiting inflammatory bone loss in patients with chronic inflammatory arthritis...
  55. ncbi I{kappa}B kinase (IKK){beta}, but not IKK{alpha}, is a critical mediator of osteoclast survival and is required for inflammation-induced bone loss
    Maria Grazia Ruocco
    Laboratory of Gene Regulation and Signal Transduction, Department of Pharmacology, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA
    J Exp Med 201:1677-87. 2005
    ..IKKbeta also protects osteoclasts and their progenitors from tumor necrosis factor alpha-induced apoptosis, and its loss in hematopoietic cells prevents inflammation-induced bone loss...
  56. ncbi High-sensitivity C-reactive protein and risk of nontraumatic fractures in the Bruneck study
    Georg Schett
    Department of Internal Medicine III and Institute for Clinical Immunology, University of Erlangen Nuremberg, Erlangen, Germany
    Arch Intern Med 166:2495-501. 2006
    ..It is unknown, however, whether low-grade inflammation in healthy individuals, as estimated by the high-sensitivity C-reactive protein (hs-CRP) level, interferes with bone metabolism and affects the risk of nontraumatic fractures...
  57. ncbi Dickkopf-1 is a master regulator of joint remodeling
    Danielle Diarra
    Department of Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen Nurnberg, Krankenhausstrasse 12, D 91054 Erlangen, Germany
    Nat Med 13:156-63. 2007
    ..We identified tumor necrosis factor-alpha (TNF) as a key inducer of DKK-1 in the mouse inflammatory arthritis model and in human rheumatoid arthritis. These results suggest that the Wnt pathway is a key regulator of joint remodeling...
  58. ncbi Anti-tumour necrosis factor alpha therapy in patients with impaired renal function
    Axel J Hueber
    Ann Rheum Dis 66:981-2. 2007
  59. ncbi RANKL is a marker and mediator of local and systemic bone loss in two rat models of inflammatory arthritis
    Marina Stolina
    Department of Metabolic Disorders, Amgen Inc, Thousand Oaks, California 91320, USA
    J Bone Miner Res 20:1756-65. 2005
    ..RANKL inhibition through OPG prevented local and systemic bone loss in these arthritis models, suggesting that RANKL inhibition is a promising new approach for treating bone loss in arthritis...
  60. ncbi The molecular scaffold Gab2 is a crucial component of RANK signaling and osteoclastogenesis
    Teiji Wada
    Institute of Molecular Biotechnology of the Austrian Academy of Sciences, Dr Bohrgasse 3 5, A 1030 Vienna, Austria
    Nat Med 11:394-9. 2005
    ..We have thus identified a new, key regulatory scaffold molecule, Gab2, that controls select RANK signaling pathways and is essential for osteoclastogenesis and bone homeostasis...
  61. ncbi The role of Wnt proteins in arthritis
    Georg Schett
    Department of Internal Medicine 3, University of Erlangen Nuremberg, Erlangen, Germany
    Nat Clin Pract Rheumatol 4:473-80. 2008
    ..It also addresses the role of Wnt in determining the differences in clinical presentation of inflammatory arthropathies and discusses implications for future therapy...
  62. ncbi Cytokines in the pathogenesis of rheumatoid arthritis
    Iain B McInnes
    Centre for Rheumatic Diseases, Glasgow Biomedical Research Centre, University of Glasgow, 120 University Place, Glasgow G12 8TA, UK
    Nat Rev Immunol 7:429-42. 2007
    ..Here, we discuss the crucial effector function of cytokines in the immunological processes that are central to the pathogenesis of rheumatoid arthritis...
  63. ncbi Remission of demyelinating polyneuropathy with immunoadsorption, low dose corticosteroids and anti-CD20 monoclonal antibody
    Jürgen Rech
    Medical Department III, University of Erlangen Nuremberg, Erlangen, Germany
    Ther Apher Dial 12:205-8. 2008
    ..Immunoadsorption in combination with a monoclonal anti-CD20 antibody in patients with demyelinating polyneuropathy with anti-MAG is effective and can be used an alternative treatment option in patients with progressive disease...
  64. ncbi Association of serum-soluble heat shock protein 60 with carotid atherosclerosis: clinical significance determined in a follow-up study
    Qingzhong Xiao
    Department of Cardiac and Vascular Sciences, St George s University of London, United Kingdom
    Stroke 36:2571-6. 2005
    ..In the current evaluation, we tested the hypothesis that sHSP60 levels are associated with the progression of carotid arteriosclerosis, prospectively...
  65. ncbi Analysis of the kinetics of osteoclastogenesis in arthritic rats
    Georg Schett
    Amgen, Inc, Thousand Oaks, California 91320, USA
    Arthritis Rheum 52:3192-201. 2005
    ..These data indicate that anti-resorptive therapies may provide the most effective bone protection, when treatment is started soon after the onset of arthritis...
  66. ncbi Hypoxia-induced increase in the production of extracellular matrix proteins in systemic sclerosis
    Jörg H W Distler
    Center of Experimental Rheumatology and Zurich Center of Integrative Human Physiology, University Hospital Zurich, Gloriastrasse 25, Zurich, Switzerland
    Arthritis Rheum 56:4203-15. 2007
    ..Based on the severely decreased oxygen levels in the skin of patients with SSc, we aimed to investigate the role of hypoxia in the pathogenesis of SSc...
  67. ncbi The osteoprotegerin/RANK/RANKL system: a bone key to vascular disease
    Stefan Kiechl
    Medical University Innsbruck, Department of Neurology, Anichstr 35, A 6020 Innsbruck, Austria
    Expert Rev Cardiovasc Ther 4:801-11. 2006
    ..RANKL in turn may be a suitable target for novel therapies. Pharmacological strategies for specific interference with the OPG/RANK/RANKL axis are currently being developed and evaluated in osteoporosis therapy...
  68. ncbi Bone histomorphometry in arthritis models
    Georg Schett
    Methods Mol Med 135:269-83. 2007
    ..Finally, evaluation of arthritic paw sections by histomorphometry, a semiautomated computerized method to measure areas of interest, is described...
  69. ncbi Cells of the synovium in rheumatoid arthritis. Osteoclasts
    Georg Schett
    Department of Internal Medicine III and Institute for Clinical Immunology, University of Erlangen Nuremberg, Erlangen, Germany
    Arthritis Res Ther 9:203. 2007
    ..Osteoclasts thus represent a link between joint inflammation and structural damage since they resorb mineralized tissue adjacent to the joint and destroy the joint architecture...
  70. ncbi Erosive arthritis
    Georg Schett
    Department of Internal Medicine 3, University of Erlangen Nurnberg, Erlangen, Germany
    Arthritis Res Ther 9:S2. 2007
    ..Blockade of osteoclast formation is thus a key strategy in preventing structural damage in arthritis. Denosumab, a humanized antibody that neutralizes RANKL, is an attractive candidate agent to inhibit inflammatory bone loss...
  71. ncbi Clinical images: rheumatologic irony
    Jochen Zwerina
    University of Erlangen, Erlangen, Germany
    Arthritis Rheum 56:1463. 2007
  72. ncbi Soluble receptor activator of nuclear factor-kappa B ligand and risk for cardiovascular disease
    Stefan Kiechl
    Department of Neurology, Innsbruck Medical University, Anichstr 35, A 6020 Innsbruck, Austria
    Circulation 116:385-91. 2007
    ....