New insights in synovial angiogenesis

Z. Szekanecz, Timea Besenyei, G. Paragh, Alisa E. Koch

Research output: Contribution to journalArticle

57 Citations (Scopus)

Abstract

Angiogenesis is the formation of new capillaries from pre-existing vessels. A number of soluble and cell-bound factors may stimulate neovascularization. The perpetuation of angiogenesis involving numerous soluble and cell surface-bound mediators has been associated with rheumatoid arthritis (RA). These angiogenic mediators, among others, include growth factors, primarily vascular endothelial growth factor (VEGF) and hypoxia-inducible factors (HIFs), as well as pro-inflammatory cytokines, various chemokines, cell adhesion molecules, proteases and others. Among the several potential angiogenesis inhibitors, targeting of VEGF, HIF-1, angiopoietin and the αVβ3 integrin, as well as some endogenous or synthetic compounds including angiostatin, endostatin, paclitaxel, fumagillin analogues, 2-methoxyestradiol and thalidomide seems to be promising for the management of synovial inflammation and angiogenesis. A complete review of antiangiogenic drugs used in animal models of arthritis or human RA is available in a table.

Original languageEnglish
Pages (from-to)13-19
Number of pages7
JournalJoint Bone Spine
Volume77
Issue number1
DOIs
Publication statusPublished - Jan 2010

Fingerprint

Vascular Endothelial Growth Factor A
Rheumatoid Arthritis
Angiostatins
Angiopoietins
Endostatins
Hypoxia-Inducible Factor 1
Thalidomide
Angiogenesis Inhibitors
Cell Adhesion Molecules
Paclitaxel
Chemokines
Integrins
Arthritis
Intercellular Signaling Peptides and Proteins
Peptide Hydrolases
Animal Models
Cell Count
Cytokines
Inflammation
Pharmaceutical Preparations

Keywords

  • Angiogenesis
  • Angiostasis
  • Rheumatoid arthritis
  • Vascular endothelial growth factor

ASJC Scopus subject areas

  • Rheumatology

Cite this

New insights in synovial angiogenesis. / Szekanecz, Z.; Besenyei, Timea; Paragh, G.; Koch, Alisa E.

In: Joint Bone Spine, Vol. 77, No. 1, 01.2010, p. 13-19.

Research output: Contribution to journalArticle

Szekanecz, Z. ; Besenyei, Timea ; Paragh, G. ; Koch, Alisa E. / New insights in synovial angiogenesis. In: Joint Bone Spine. 2010 ; Vol. 77, No. 1. pp. 13-19.
@article{f7cbf86dea3949caa540f096ae943665,
title = "New insights in synovial angiogenesis",
abstract = "Angiogenesis is the formation of new capillaries from pre-existing vessels. A number of soluble and cell-bound factors may stimulate neovascularization. The perpetuation of angiogenesis involving numerous soluble and cell surface-bound mediators has been associated with rheumatoid arthritis (RA). These angiogenic mediators, among others, include growth factors, primarily vascular endothelial growth factor (VEGF) and hypoxia-inducible factors (HIFs), as well as pro-inflammatory cytokines, various chemokines, cell adhesion molecules, proteases and others. Among the several potential angiogenesis inhibitors, targeting of VEGF, HIF-1, angiopoietin and the αVβ3 integrin, as well as some endogenous or synthetic compounds including angiostatin, endostatin, paclitaxel, fumagillin analogues, 2-methoxyestradiol and thalidomide seems to be promising for the management of synovial inflammation and angiogenesis. A complete review of antiangiogenic drugs used in animal models of arthritis or human RA is available in a table.",
keywords = "Angiogenesis, Angiostasis, Rheumatoid arthritis, Vascular endothelial growth factor",
author = "Z. Szekanecz and Timea Besenyei and G. Paragh and Koch, {Alisa E.}",
year = "2010",
month = "1",
doi = "10.1016/j.jbspin.2009.05.011",
language = "English",
volume = "77",
pages = "13--19",
journal = "Revue du Rhumatisme (English Edition)",
issn = "1169-8446",
publisher = "Elsevier Masson",
number = "1",

}

TY - JOUR

T1 - New insights in synovial angiogenesis

AU - Szekanecz, Z.

AU - Besenyei, Timea

AU - Paragh, G.

AU - Koch, Alisa E.

PY - 2010/1

Y1 - 2010/1

N2 - Angiogenesis is the formation of new capillaries from pre-existing vessels. A number of soluble and cell-bound factors may stimulate neovascularization. The perpetuation of angiogenesis involving numerous soluble and cell surface-bound mediators has been associated with rheumatoid arthritis (RA). These angiogenic mediators, among others, include growth factors, primarily vascular endothelial growth factor (VEGF) and hypoxia-inducible factors (HIFs), as well as pro-inflammatory cytokines, various chemokines, cell adhesion molecules, proteases and others. Among the several potential angiogenesis inhibitors, targeting of VEGF, HIF-1, angiopoietin and the αVβ3 integrin, as well as some endogenous or synthetic compounds including angiostatin, endostatin, paclitaxel, fumagillin analogues, 2-methoxyestradiol and thalidomide seems to be promising for the management of synovial inflammation and angiogenesis. A complete review of antiangiogenic drugs used in animal models of arthritis or human RA is available in a table.

AB - Angiogenesis is the formation of new capillaries from pre-existing vessels. A number of soluble and cell-bound factors may stimulate neovascularization. The perpetuation of angiogenesis involving numerous soluble and cell surface-bound mediators has been associated with rheumatoid arthritis (RA). These angiogenic mediators, among others, include growth factors, primarily vascular endothelial growth factor (VEGF) and hypoxia-inducible factors (HIFs), as well as pro-inflammatory cytokines, various chemokines, cell adhesion molecules, proteases and others. Among the several potential angiogenesis inhibitors, targeting of VEGF, HIF-1, angiopoietin and the αVβ3 integrin, as well as some endogenous or synthetic compounds including angiostatin, endostatin, paclitaxel, fumagillin analogues, 2-methoxyestradiol and thalidomide seems to be promising for the management of synovial inflammation and angiogenesis. A complete review of antiangiogenic drugs used in animal models of arthritis or human RA is available in a table.

KW - Angiogenesis

KW - Angiostasis

KW - Rheumatoid arthritis

KW - Vascular endothelial growth factor

UR - http://www.scopus.com/inward/record.url?scp=73449125837&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=73449125837&partnerID=8YFLogxK

U2 - 10.1016/j.jbspin.2009.05.011

DO - 10.1016/j.jbspin.2009.05.011

M3 - Article

C2 - 20022538

AN - SCOPUS:73449125837

VL - 77

SP - 13

EP - 19

JO - Revue du Rhumatisme (English Edition)

JF - Revue du Rhumatisme (English Edition)

SN - 1169-8446

IS - 1

ER -