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1.

001-es BibID:BIBFORM015870
Első szerző:Szekanecz Zoltán (reumatológus, belgyógyász, immunológus)
Cím:Angiogenesis and vasculogenesis in rheumatoid arthritis / Szekanecz, Z., Besenyei, T., Szentpetery, A., Koch, A. E.
Dátum:2010
ISSN:1531-6963 (Electronic)
Megjegyzések:Angiogenesis is the formation of new capillaries from pre-existing vessels, whereas vasculogenesis is de-novo capillary formation from endothelial precursor cells (EPCs). Current understanding of the role of angiogenesis and vasculogenesis in rheumatoid arthritis (RA) and possibilities of therapeutic intervention should be summarized. RECENT FINDINGS: There have been many recent studies on the role of the hypoxia and hypoxia-inducible factor (HIF)-vascular endothelial growth factor (VEGF)-angiopoietin axis in angiogenesis associated with RA. The role of additional growth factors, chemokines, cytokines, matrix components and adhesion molecules has been further characterized. Macrophage migration inhibitory factor (MIF) may link inflammation, angiogenesis and atherosclerosis. Junctional adhesion molecules (JAMs) and focal adhesion kinases (FAKs) have recently been implicated in inflammatory angiogenesis. Novel information regarding the role of serum amyloid A (SAA) and sphingosine kinase has become available. Most of these angiogenic factors have recently been targeted using various techniques and arthritis models. Whereas angiogenesis is abundant in RA, there is defective EPC function and vasculogenesis leading to atherosclerosis and vascular disease in arthritis. Treatment with EPCs already under investigation in vascular diseases may also be attempted in RA. SUMMARY: Targeting angiogenesis and restoration of vasculogenesis may be beneficial for the therapy and outcome of RA.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Angiogenesis Inhibitors/pharmacology/therapeutic use
Angiogenic Proteins/antagonists & inhibitors/metabolism
Arthritis/complications/metabolism/physiopathology
Arthritis, Rheumatoid/*complications/metabolism/*physiopathology
Blood Vessels/drug effects/metabolism/physiopathology
Endothelial Cells/drug effects/immunology/metabolism
Humans
Neovascularization, Pathologic/drug therapy/*immunology/*physiopathology
Vascular Diseases/drug therapy/*immunology/*physiopathology
Megjelenés:Current Opinion in Rheumatology. - 22 : 3 (2010), p. 299-306. -
További szerzők:Besenyei Tímea (1980-) (reumatológus, belgyógyász) Szentpétery Ágnes (1978-) (reumatológus) Koch, Alisa E.
Internet cím:DOI
elektronikus változat
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2.

001-es BibID:BIBFORM007113
Első szerző:Szekanecz Zoltán (reumatológus, belgyógyász, immunológus)
Cím:Chemokines and angiogenesis / Szekanecz, Z., Koch, A. E.
Dátum:2001
ISSN:1040-8711 (Print)
Megjegyzések:Chemokines mediate the ingress of leukocytes, including neutrophils and monocytes, into the inflamed synovium. Among the four known chemokine families, C-X-C and C-C chemokines seem to be of outstanding importance in this process. Angiogenesis, the formation of new vessels, is also important in the pathogenesis of rheumatoid arthritis. In this review, the authors discuss the role of the most important chemokines in the pathogenesis of rheumatoid synovitis. The most relevant angiogenic factors and angiogenesis inhibitors involved in rheumatoid arthritis are also discussed. Because certain chemokines may also play a role in neovascularization, chemokines and the process of angiogenesis are described in this context as well. Apart from discussing the pathogenic role of these factors, the authors also review the important relevance of chemokines and angiogenesis for therapeutic intervention.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Antibodies
Arthritis, Rheumatoid
Chemokines
Humans
Neovascularization, Pathologic
Receptors, Chemokine
Megjelenés:Current Opinion in Rheumatology. - 13 : 3 (2001), p. 202-208. -
További szerzők:Koch, Alisa E.
Internet cím:elektronikus változat
elektronikus változat
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3.

001-es BibID:BIBFORM007121
Első szerző:Szekanecz Zoltán (reumatológus, belgyógyász, immunológus)
Cím:Macrophages and their products in rheumatoid arthritis / Szekanecz, Z., Koch, A. E.
Dátum:2007
ISSN:1040-8711 (Print)
Megjegyzések:Macrophages differentiate from peripheral-blood monocytes. Both monocytes and synovial macrophages are key players in rheumatoid arthritis. These cells are involved in the initiation and perpetuation of inflammation, leukocyte adhesion and migration, matrix degradation and angiogenesis. Macrophages express adhesion molecules, chemokine receptors and other surface antigens. They also secrete a number of chemokines, cytokines, growth factors, proteases and other mediators. RECENT FINDINGS: Macrophage migration-inhibitory factor has drawn significant attention recently. This cytokine is involved in macrophage activation and cytokine production. Migration-inhibitory factor also regulates glucocorticoid sensitivity and may be a pathogenic link between rheumatoid arthritis and atherosclerosis. Novel macrophage-derived chemokines and chemokine receptors have been identified. Interleukin-10 may have several proinflammatory effects that may influence its action in rheumatoid arthritis. Several proteinases including cathepsin G are produced by macrophages during rheumatoid arthritis-associated inflammatory and angiogenic events. Antirheumatic drugs, imatinib, chemokine receptor inhibitors and other specific strategies may become included in the therapy of rheumatoid arthritis. SUMMARY: Macrophages and their products are key players in the pathogenesis of rheumatoid arthritis and may be good therapeutic targets.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Animals
Antirheumatic Agents
Apoptosis
Arthritis, Experimental
Arthritis, Rheumatoid
Cell Adhesion Molecules
Cell Differentiation
Chemokines
Cytokines
Growth Substances
Humans
Macrophages
Mice
Neovascularization, Pathologic
Osteoclasts
Peptide Hydrolases
Protease Inhibitors
Receptors, Chemokine
Megjelenés:Current Opinion in Rheumatology. - 19 : 3 (2007), p. 289-295. -
További szerzők:Koch, Alisa E.
Internet cím:elektronikus változat
DOI
elektronikus változat
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