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Angiogenesis: general mechanisms and implications for rheumatoid arthritis
1Service de rhumatologie, centre hospitalo-universitaire and INSERM U479, Faculté Xavier Bichat, Paris, France.
Joint Bone Spine
|January 6, 2001
Summary
Rheumatoid arthritis involves inflammation targeting blood vessels, promoting pannus growth and joint damage. Angiogenesis inhibitors show promise in animal models, suggesting potential human therapies for this condition.
Area of Science:
- Vascular biology
- Rheumatology
- Immunology
Background:
- The vascular endothelium is a key target in rheumatoid arthritis (RA), regulating inflammatory cell and molecule trafficking to synovial tissue.
- Local blood vessel proliferation contributes to pannus formation, driving cartilage and bone destruction in RA.
- Angiogenesis, the formation of new blood vessels, is a critical process in RA pathogenesis.
Purpose of the Study:
- To review the role of angiogenesis in rheumatoid arthritis.
- To discuss the potential of angiogenesis inhibitors as a therapeutic strategy for RA.
Main Methods:
- Review of existing literature on angiogenesis in rheumatoid arthritis.
- Analysis of data from animal models of arthritis regarding angiogenesis inhibitors.
Main Results:
- Angiogenesis involves numerous factors including cytokines, chemokines, growth factors, adhesion molecules, proteinases, and matrix proteins.
- In animal models, angiogenesis inhibitors have demonstrated improvements in clinical and radiological outcomes of arthritis.
Conclusions:
- Angiogenesis is a significant factor in rheumatoid arthritis pathogenesis.
- Angiogenesis inhibitors represent a potential therapeutic avenue for human RA, warranting further investigation.
- Continued research into the mechanisms regulating angiogenesis is crucial for therapeutic development.
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