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MeSH Review:

Choroidal Neovascularization

Gehlbach, P. et al., Spilsbury, K. et al., Rasmussen, H. et al., Matsuda, S. et al., Das, A. et al., et al.

Rakic, Lambert, Devy, Luttun, Carmeliet, Claes, Nguyen, Foidart, Noël, Munaut, Ruiz-Moreno, de la Vega, Ruiz-Moreno, Alió, Lambert, Munaut, Jost, Noël, Werb, Foidart, Rakic, Rakic, Lambert, Munaut, Bajou, Peyrollier, Alvarez-Gonzalez, Carmeliet, Foidart, Noël, Cousins, Espinosa-Heidmann, Csaky, Robinson, Baffi, Yuan, Sung, Byrnes, Cox, Csaky, Yanagi, Tamaki, Obata, Muranaka, Homma, Matsuoka, Mano, Das, Boyd, Jones, Talarico, McGuire, Vinores, Xiao, Aslam, Shen, Oshima, Nambu, Liu, Carmeliet, Campochiaro, Lambert, Munaut, Noël, Frankenne, Bajou, Gerard, Carmeliet, Defresne, Foidart, Rakic,

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Disease relevance of Choroidal Neovascularization

Up-regulated basolateral VEGF secretion by RPE in hypoxia or loss of polarity of VEGF production may play a role in the pathogenesis of choroidal neovascularization [1].
These data suggest that periocular gene transfer of sFlt-1 should be considered for treatment of choroidal neovascularization and diabetic macular edema [2].
In three murine disease models (the laser-induced choroidal neovascularization model, the VEGF transgenic model, and the retinopathy of prematurity model) significant inhibition of neovascularization (up to 85%) was demonstrated with doses of Ad(GV)PEDF vectors ranging from 1 x 10(8) to 1 x 10(9) pu [3].
Increased expression of Ang1 in eyes with severe retinal ischemia or in eyes with rupture of Bruch's membrane significantly suppressed the development of retinal or choroidal neovascularization, respectively [4].
Expression of mutant fibulin proteins may contribute to macular degeneration and choroidal neovascularization by causing ER stress leading to RPE dysfunction and increased VEGF expression [5].

High impact information on Choroidal Neovascularization

TIMP3, which encodes a potent angiogenesis inhibitor, is mutated in Sorsby fundus dystrophy, a macular degenerative disease with submacular choroidal neovascularization [6].
Here we report that choroidal neovascularization (CNV) incited by injury was increased by excess VEGF-A before injury but was suppressed by VEGF-A after injury [7].
Drusen complement components C3a and C5a promote choroidal neovascularization [8].
Influence of plasminogen activator inhibitor type 1 on choroidal neovascularization [9].
In mice deficient in MMP-9 expression the development of choroidal neovascularization induced by laser photocoagulation still occurred, but at a reduced level [10].

Chemical compound and disease context of Choroidal Neovascularization

Nitric oxide (NO) promotes retinal and choroidal neovascularization, although different isoforms of nitric-oxide synthetase (NOS) are critical in each [11].
The same treatment reduced the incidence and extent of sodium fluorescein leakage from choroidal neovascular lesions by 52% (p < 0.05) and 36% (p < 0.01), respectively, in a laser-induced murine choroidal neovascularization model [12].
On day 14, fluorescein angiography was performed to detect choroidal neovascularization [13].
Subconjunctival administration of bucillamine suppresses choroidal neovascularization in rat [14].
After intravenous injection of each liposome, TTT with the modified slit lamp was performed on normal rat choroid or tissue with choroidal neovascularization (CNV) [15].

Biological context of Choroidal Neovascularization

Periocular delivery offers potential advantages over other routes of delivery and the demonstration that sFlt-1 enters the eye from the periocular space in sufficient levels to achieve efficacy in treating choroidal neovascularization and retinal vascular permeability is a novel finding that has important clinical implications [2].
Implication of the hypoxia response element of the Vegf promoter in mouse models of retinal and choroidal neovascularization, but not retinal vascular development [16].
MAIN OUTCOME MEASURES: Clinical and angiographic records were analyzed for evidence of changes in visual acuity, clinically evident subretinal fluid and the extent of fluorescein leakage from choroidal neovascularization (CNV) [17].
Peak-time delays at 15 minutes and 24 hours may be caused by other factors, such as increased intracellular calcium (Ca(2+)), the release of nitric oxide or heat shock proteins, vasodilation, or change in choroidal neovascularization [18].
Safety and pharmacokinetics of intravitreal 2-methoxyestradiol implants in normal rabbit and pharmacodynamics in a rat model of choroidal neovascularization [19].

Anatomical context of Choroidal Neovascularization

These results show that even temporary overexpression of VEGF in retinal pigment epithelial cells is sufficient to induce choroidal neovascularization in the rat eye [20].
Overexpression of vascular endothelial growth factor (VEGF) in the retinal pigment epithelium leads to the development of choroidal neovascularization [20].
Integrin alphavbeta3 has been reported to be strongly expressed in vascular endothelial cells of surgically excised choroidal neovascular membranes and is thought to be a potential antigen for mAb-mediated drug targeting of choroidal neovascularization (CNV) [21].
PURPOSE: To investigate the role of the leukocyte adhesion molecules CD18 and intercellular adhesion molecule (ICAM)-1 in the development of choroidal neovascularization (CNV) [22].
Patients with monocytes that expressed the greatest amount of TNF-alpha demonstrated higher prevalence of choroidal neovascularization [23].

Gene context of Choroidal Neovascularization

Mice without uPA, tPA, or plasminogen genes are resistant to experimental choroidal neovascularization [24].
Because VEGF is a major cytokine involved in angiogenesis, and CTGF is a main cytokine related to fibrosis, these results suggest that changes in their expression may be important mechanisms underlying the decreased choroidal neovascularization and fibrosis after administration of TA [25].
In the current study, the influence of placental growth factor (PlGF), a member of the VEGF family, in human and experimental choroidal neovascularization (CNV) was investigated [26].
These two ABCA4 alleles were slightly more frequent in patients with AMD with choroidal neovascularization (2.7%) than those without this complication (2.5%) [27].
MMP-2 and MMP-9 synergize in promoting choroidal neovascularization [28].

Analytical, diagnostic and therapeutic context of Choroidal Neovascularization

METHODS: The expression of PA members mRNA was evaluated in human and experimental choroidal neovascularization (CNV) by RT-PCR [24].
Dose-dependent modulation of choroidal neovascularization by plasminogen activator inhibitor type I: implications for clinical trials [29].
CONCLUSION: Large-spot size transpupillary thermotherapy is effective in stabilizing the visual acuity in those patients who have occult choroidal neovascularization due to age-related macular degeneration [30].
PURPOSE: To analyze the appearance, incidence, and characteristics of choroidal neovascularization (CNV) in patients with high myopia corrected by implantation of a phakic anterior chamber intraocular lens (PACL) [31].
OBJECTIVES: To determine the role played by the urokinase plasminogen activator (uPA) and urokinase plasminogen activator receptor (uPAR) system in choroidal neovascularization (CNV) and whether inhibition of this system can suppress the extent of CNV in an animal model [32].

References

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