الفهرس يوجد فقط 14 صفحة متاحة للعرض العام
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المستخلص
Ocular neovascularization is the fundamental pathology in the form of abnormal angiogenesis that leads to vision loss in a wide range of ocular diseases. The most frequent sites of ocular neovascularization are:
1- Choroidal: as in wet Age related macular degeneration and pathologic (progressive) myopia.
2- Retinal: as in proliferative diabetic retinopathy, central and branch retinal vein occlusion and retinopathy of prematurity.
3- Corneal: due to ischemia, trauma, infections, keratoplasty and interstitial keratitis.
A number of cytokines and growth factors that activate endothelial cells were found to modulate the formation and regression of the abnormal vessels in this process. Under certain pathological circumstances such as hypoxia, ischemia, inflammation, infection and trauma, the balance between angiogenic stimulators and angiogenic inhibitors is disturbed, leading to the formation of new vessels.
Vascular endothelial growth factor (VEGF) has been demonstrated in multiple studies to be necessary and central to the process of ocular neovascularization. VEGF binds to two receptor tyrosine kinases: VEGF receptor (VEGFR)-1 and VEGFR-2. Another receptor (VEGFR-3) involved in the regulation of the lymphatic system.
It was found that VEGF inhibition can effectively abolish the neovascular process. Targeting VEGF includes:
1- Monoclonal antibodies directed against VEGF.
2- Targeting its receptors: VEGFR-1 and VEGFR-2. or
3- Small molecule tyrosine kinase inhibitors that act intracellularly to prevent autophosphorylation and activation of downstream growth –promoting signaling cascades.
Examples of anti-VEGF therapies