Subfoveal fibrovascular membranes in age-related macular degeneration express vascular endothelial growth factor

Potential long-term inhibition of ocular neovascularisation by recombinant adeno-associated virus-mediated secretion gene therapy

“…28,36 It is widely believed that VEGF up-regulation also plays a major part in the development of ocular NV. [6][7][8][9][20][21][22] Several studies have further shown that inhibition of VEGF activity by administration of VEGF-specific kinase inhibitors, VEGF antibodies, VEGF receptors and VEGF antisense oligonucleotides successfully suppressed the development of retinal and choroidal NV. [37][38][39][40] In particular, Honda et al 41 showed that expression of adenovirus-mediated sFlt-1 suppressed choroidal NV.…”

“…The up-regulation of VEGF and its receptors in human neovascular ocular tissues has been well documented. [6][7][8][9][10][11] Several studies have further shown that overexpression of VEGF in the retina by adenoviral vectors or in transgenic animal models resulted in retinal and choroidal NV. [12][13][14] Current conventional treatments of retinal and choroidal NV such as laser photocoagulation and surgical intervention provide only symptomatic treatment of the disease without addressing the underlying cause.…”

Novel anti-VEGF chimeric molecules delivered by AAV vectors for inhibition of retinal neovascularization

“…1 Formation of new blood vessels caused by the overproduction of growth factors such as VEGF is a key component of diseases such as wet age-related macular degeneration (AMD), proliferative diabetic retinopathy (PDR) and tumor growth. [2][3][4] Blocking of VEGF with antibodies, soluble VEGF receptors (sVEGFR) or inhibition of VEGF receptor (VEGFR) tyrosine kinase activity are useful strategies that have shown promising preclinical and clinical results. [4][5][6] Ranibizumab, an anti-VEGF drug given intravitreally to wet-AMD patients results in substantially improved visual acuity.…”

Inhibitory efficacy of hypoxia-inducible factor 1α short hairpin RNA plasmid DNA-loaded poly (D, L-lactide-co-glycolide) nanoparticles on choroidal neovascularization in a laser-induced rat model

“…14 Clinical studies have shown that the age-related changes in Bruch's membrane and the dropout of choriocapillaris cause impaired diffusion of oxygen. 15,16 Outer retina hypoxia 17 and the resulting transcriptional activation of the HIF-1 [18][19][20] may become an important driving force of CNV formation by stimulating VEGF overexpression, 21,22 in addition to the effects of increased oxidative stress and low-grade inflammation. Recently, it has also been shown that CNV membranes are positive for HIF-1 expression, and this expression tends to be localized to the retinal pigment epithelium (RPE) cells.…”