| Autor: |
Tombrain-Tink, Joyce, Barnstable, Colin J., Robertson, Stella M., Davis, Alberta A., Dahlin, David C., Clark, Abbot F. |
| Zdroj: |
Ocular Angiogenesis; 2006, p341-354, 14p |
| Abstrakt: |
A variety of angiogenic factors have been identified in choroidal neovascularization (CNV) membranes of patients with exudative age-related macular degeneration (AMD) (1), and several different angiogenic factors can cause experimental CNV (2,3). One of the rate-limiting steps for neovascularization is the angiogenic factor-induced activation of vascular endothelial cells and induction of the angiogenic proteolytic cascade, which allows the endothelial cells to break through the vessel wall and migrate through interstitial tissue to form new blood vessels. An ideal therapeutic agent for the treatment of exudative AMD should be able to inhibit CNV independent of the factor(s) inducing neovascularization and should attack the rate-limiting step of neovascularization. In addition, this agent should be locally administered via a mechanism that does not pierce the eye, deliver the therapeutic agent to the macula, and not require frequent administration. Due to the chronic nature of AMD, the therapeutic agent should have superior ocular and systemic safety. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Supplemental Index |
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