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Results for “Retinal Neovascularization”

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PubMed2004

Incidence of patients presenting with exudative maculopathy and neovascular retinal disease in an urban population.

PURPOSE: To determine the incidence of exudative macular and neovascular retinal disease presenting within a defined urban population. STUDY DESIGN: prospective, observational, consecutive case series. PATIENTS AND METHODS: Patients referred to ten ophthalmic centers within a defined 10-week period with a newly diagnosed exudative macular and/or neovascular retinal disease were examined fundoscopically, angiographically and quantified according to age and underlying disease. RESULTS: A total of 527 eyes of 426 patients were referred. The most frequent disease was neovascular age-related macular degeneration (AMD, 199/527, 37.8%, 184 patients), followed by diabetic maculopathy and/or proliferative diabetic retinopathy (199/527, 37.8%, 128 patients) and venous occlusive disease (67/527, 12.7%, 67 patients). The majority of neovascular AMD consisted of occult without classic choroidal neovascularization (CNV, 115/ 199, 57.8%); predominantly classic CNV was seen more often than minimally classic CNV (43/199, 21.6% vs. 27/ 199, 13.6%). The overwhelming majority of the diabetic cases had diabetic macular edema (179/199, 89.9%); only 10.1% had vasoproliferative disease. All other causes of CNV, macular edema/exudation, and retinal neovascularization were observed in < 5% of all patients. CONCLUSION: The main causes of exudative maculopathy are CNV due to neovascular AMD and diabetic macular edema. Proliferative diabetic retinopathy is the main cause of retinal neovascularization. The number of patients with neovascular AMD presents a future challenge for ophthalmologists.

Aged↗

PubMed1996

Oligodeoxynucleotides inhibit retinal neovascularization in a murine model of proliferative retinopathy.

Diseases characterized by retinal neovascularization are among the principal causes of visual loss worldwide. The hypoxia-stimulated expression of vascular endothelial growth factor (VEGF) has been implicated in the proliferation of new blood vessels. We have investigated the use of antisense phosphorothioate oligodeoxynucleotides against murine VEGF to inhibit retinal neovascularization and VEGF synthesis in a murine model of proliferative retinopathy. Intravitreal injections of two different antisense phosphorothioate oligodeoxynucleotides prior to the onset of proliferative retinopathy reduced new blood vessel growth a mean of 25 and 31% compared with controls. This inhibition was dependent on the concentration of antisense phosphorothioate oligodeoxynucleotides and resulted in a 40-66% reduction in the level of VEGF protein, as determined by Western blot analysis. Control (sense, nonspecific) phosphorothioate oligodeoxynucleotides did not cause a significant reduction in retinal neovascularization or VEGF protein levels. These data further establish a fundamental role for VEGF expression in ischemia-induced proliferative retinopathies and a potential therapeutic use for antisense phosphorothioate oligodeoxynucleotides.

Animals↗

PubMed2001

Unilateral retinal vasculitis, branch retinal artery occlusion and subsequent retinal neovascularization in Crohn's disease.

PURPOSE: To report on a case of Crohn's disease and unilateral retinal vasculitis, branch retinal artery occlusion and subsequent retinal neovascularization. METHODS: We examined a 38-year-old woman with severe left visual loss and biopsy-proven Crohn's disease diagnosed four years prior to the ocular involvement. A Heidelberg scanning laser ophthalmoscope was used for fundus fluorescein angiography and indocyanine green angiography. Retinal neovascularization was detected during the follow-up. RESULTS: Successful regression of retinal neovascularization was achieved after argon green laser panretinal photocoagulation in addition to oral steroid and salazopyrine. CONCLUSION: Retinal vascular involvement is a rare ocular feature of Crohn's disease and may result in retinal neovascularization that may necessitate prompt laser photocoagulation.

Adult↗

PubMed2002

Pigment epithelium-derived factor suppresses ischemia-induced retinal neovascularization and VEGF-induced migration and growth.

PURPOSE: To determine the effect of pigment epithelium-derived factor (PEDF) in a mouse model of ischemia-induced retinal neovascularization and on vascular endothelial growth factor (VEGF)--induced migration and growth of cultured microvascular endothelial cells. METHODS: Human recombinant PEDF was expressed in the human embryonic kidney 293 cell line and purified by ammonium sulfate precipitation and cation exchange chromatography. C57BL/6 mice were exposed to 75% oxygen from postnatal day (P)7 to P12 and then returned to room air. Mice received intravitreal injections of 2 microg PEDF in one eye and vehicle in the contralateral eye on P12 and P14. At P17, mice were killed and eyes enucleated for quantitation of retinal neovascularization. The mitogenic and motogeneic effects of VEGF on cultured bovine retinal and adrenal capillary endothelial cells were examined in the presence or absence of PEDF, using cell counts and migration assays. RESULTS: Two species of human recombinant PEDF, denoted A and B, were purified to apparent homogeneity. PEDF B appeared to comigrate on SDS-PAGE with PEDF from human vitreous samples. Changes in electrophoretic mobility after peptide-N-glycosidase F (PNGase F) digestion suggest that both PEDF forms contain N-linked carbohydrate. Analyses of the intact proteins by liquid chromatography-electrospray mass spectrometry (LC-ESMS) revealed the major molecular weight species for PEDF A (47,705 +/- 4) and B (46,757 +/- 5). LC-ESMS analysis of tryptic peptides indicated that PEDF A and B exhibit differences in glycopeptides containing N-acetylneuraminic acid (NeuAc) and N-acetylhexosamine (HexNAc). Intravitreal administration of either species of PEDF significantly inhibited retinal neovascularization (83% for PEDF A and 55% for PEDF B; P = 0.024 and 0.0026, respectively). PEDF A and B (20 nM) suppressed VEGF-induced retinal microvascular endothelial cell proliferation by 48.8% and 41.4%, respectively, after 5 days (P < 0.001) and VEGF-induced migration by 86.5% +/- 16.7% and 78.1% +/- 22.3%, respectively, after 4 hours (P = 0.004 and P = 0.008, respectively). CONCLUSIONS: These data indicate that elevated concentrations of PEDF inhibit VEGF-induced retinal endothelial cell growth and migration and retinal neovascularization. These findings suggest that localized administration of PEDF may be an effective approach for the treatment of ischemia-induced retinal neovascular disorders.

Animals↗

PubMed1998

The topographic distribution of the first sites of diabetic retinal neovascularization.

PURPOSE: To examine the topographic distribution of the origin of diabetic retinal neovascularization. METHODS: The eyes of 3,121 patients with background diabetic retinopathy were investigated. These patients were volunteers in systemic medical therapy experiments. Color stereo photographs were obtained annually. The first retinal neovascularization sites were identified and the distances from the optic nerve measured. RESULTS: In 1 year, neovascularization originated in 282 eyes. The superotemporal quadrant, at 6 mm from the optic disk, was the most frequent initial site. CONCLUSIONS: The first retinal neovascularization sites cluster around specific anatomic foci. This information should influence retinopathy monitoring protocols.

Clinical Trials as Topic↗

PubMed2004

Marked inhibition of retinal neovascularization in rats following soluble-flt-1 gene transfer.

BACKGROUND: In mouse models of retinopathy of prematurity (ROP) inhibitors of vascular endothelial growth factor (VEGF) functions administered systemically completely block retinal neovascularization. In contrast, selective ocular VEGF depletion has achieved an approx. 50% inhibition of retinal neovascular growth. It is unclear whether a more complete inhibition of new blood vessel development can be obtained with an anti-VEGF therapy localized to the eye. Therefore, the objective of the present study was to determine the effect of local anti-VEGF therapy in a different animal model which closely mimics human ROP. METHODS: Rats were exposed to alternating cycles of high and low levels of oxygen for 14 days immediately after birth; thereafter, they were intravitreally injected with an adenoviral vector expressing a secreted form of the VEGF receptor flt-1 (Ad.sflt), which acts by sequestering VEGF. Contralateral eyes were injected with the control vector carrying the reporter gene expressing beta-galactosidase (Ad.betaGal). RESULTS: At the peak of retinal neovascular growth, i.e. post-natal day 21 (P21), we observed up to 97.5% decrease in retinal neovascularization in animals injected with Ad.sflt. At the end of observation (P28), no significant difference in retinal vessel number was detected in both oxygen-injured and normoxic Ad.sflt-treated retinas compared with untreated or Ad.betaGal-treated retinas. CONCLUSION: Adenoviral-mediated sflt-1 gene transfer induces a near-complete inhibition of ischemia-induced retinal neovascularization in rats without affecting pre-existing retinal vessels.

Adenoviridae↗

PubMed2001

Colocalization of neuropilin-1 and Flk-1 in retinal neovascularization in a mouse model of retinopathy.

PURPOSE: To investigate the mechanisms of the development of retinal neovascularization, the localizations of vascular endothelial (VEGF) receptors Flk-1 and neuropilin (NP)-1 mRNAs were examined. METHODS: The model of retinopathy of prematurity (ROP) was produced by ischemia-induced ocular neovascularization, by exposing postnatal day-7 mice to 75% oxygen for 5 days and then returning them to room air for 5 days. Retinal neovascularization was visualized by injection of fluorescein-dextran. Expression of Flk-1 and NP-1 mRNAs were examined by in situ hybridization with flatmount and serial sections of the retina. The localization of NP-1 was also confirmed by immunohistochemistry. Blood vessel patterns were characterized by immunohistochemical localization of von Willebrand factor (vWF). RESULTS: Flatmount in situ hybridization showed intense expression of NP-1 and Flk-1 mRNAs colocalized in the area of neovascularization. In situ hybridization of serial sections of the retina revealed that expression of Flk-1 and NP-1 was restricted to neovascularized vessels of the retina from ROP mice. CONCLUSIONS: The restricted expression of Flk-1 and NP-1 on neovascularized vessels suggests that these molecules may play important roles in retinal neovascularization. This is the first report of the colocalization of NP-1 and Flk-1 on neovascularized vessels of the retina from ROP mice.

Animals↗

PubMed2002

Difference in ischemic regulation of vascular endothelial growth factor and pigment epithelium--derived factor in brown norway and sprague dawley rats contributing to different susceptibilities to retinal neovascularization.

The present study compared susceptibilities of Sprague Dawley (SD) and Brown Norway (BN) rats with ischemia-induced retinal neovascularization. An exposure to constant hyperoxia followed by normoxia induced significant retinal neovascularization in BN rats but not in SD rats, as demonstrated by fluorescein retinal angiography, measurement of avascular area, and count of preretinal vascular cells. These results indicate a rat strain difference in susceptibility to retinal neovascularization. To understand the molecular basis responsible for the strain difference, we have measured the levels of pigment epithelium-derived factor (PEDF), an angiogenic inhibitor, and vascular endothelial growth factor (VEGF), a major angiogenic stimulator in the retina. The hyperoxia-treated BN rats showed a significant reduction in retinal PEDF, but they showed a substantial increase of VEGF at both the protein and RNA levels, resulting in an increased VEGF-to-PEDF ratio. Hyperoxia-treated SD rats showed changes in PEDF and VEGF levels that were less in magnitude and of shorter duration than in BN rats. In age-matched normal BN and SD rats, however, there was no detectable difference in the basal VEGF-to-PEDF ratio between the strains. These observations support the idea that different regulation of angiogenic inhibitors and stimulators under ischemia are responsible for the differences in susceptibility to ischemia-induced retinal neovascularization in SD and BN rats.

Angiogenesis Inhibitors↗

PubMed1999

Suppression of retinal neovascularization by the NF-kappaB inhibitor pyrrolidine dithiocarbamate in mice.

PURPOSE: To evaluate the effect of pyrrolidine dithiocarbamate (PDTC), an inhibitor of nuclear factor kappaB (NF-kappaB), on retinal neovascularization in a murine model of ischemic retinopathy. METHODS: One-week-old C57BL/6N mice were exposed to 75%+/-2% oxygen for 5 days and then were returned to room air to induce retinal neovascularization. After the return to room air, the left and right eyes were injected intravitreally with PDTC or a vehicle, respectively. Retinal neovascularization was examined by injecting fluorescein dextran and angiography after 5 days in room air and was quantitated histologically with a masked protocol. The effects of PDTC on NF-kappaB activation were evaluated by immunohistochemistry. To examine the toxicity of PDTC, the histologic change in the retina was examined by light and electron microscopy. RESULTS: Retinal neovascularization in the eye injected with PDTC by intravitreal methods was reduced in 100% of animals compared with that apparent in the vehicle-treated eye. The inhibitory effect was dose-dependent, with a maximal inhibition of 39% (P < 0.01) at a dose of 1 nmole. The immunostaining intensity for NF-KB in the retina was reduced by PDTC injections. No side effects by PDTC in the retina were observed by light and electron microscopy. CONCLUSIONS: NF-kappaB activation appears to be required for retinal angiogenesis, given that the administration of PDTC suppressed retinal neovascularization. PDTC may prove beneficial in the treatment of ischemic neovascular diseases such as diabetic retinopathy and retinal vein occlusion.

Animals↗

PubMed1981

Retinal neovascularization after intravitreal fibroblast injection.

We have developed a new model of retinal neovascularization in the rabbit. After intravitreal autotransplantation of 250,000 tissue-cultured skin fibroblasts, we observed strand formation in the midvitreous cavity. These strands grew toward the vascularized part of the retina and attached to it. Once the attachment was established, retinal neovascularization began with growth of vessels along the fibrous strand. After three months, this retinal neovascularization regressed. The presence of immature capillaries was confirmed by electron microscopic examination. Of 43 eyes, 31 (72%) developed neovascularization.

Animals↗

PubMed2006

[Fluorescein angiography of retinal neovascularization model in mice].

OBJECTIVE: To investigate a high molecular weight fluorescein angiography in the application of retinal neovascularization model in mouse. METHODS: retinal neovascularization model was induced by exposure mouse to an environment containing high concentration of oxygen. High molecular weight fluorescein isothiocyanate dextran were perfused through the left ventricle directly, then the mouse eyes were enucleated and fixed with 4% paraformaldehyde. The retina was separated from the eyecup and flat mounting was performed on a gelatin coated slide. The vasculature was examined under fluorescent microscope. RESULT: The whole retinal vasculature was clearly visualized under fluorescent microscope. By focusing on different layer of the tissue, superficial, deep vascular plexus and connecting vessels also could be distinguished. The neovascular response occurred at the junction between the vascular and the avascular retina. CONCLUSION: High molecular weight fluorescein angiography can be applied for retinal neovascularization evaluation.

Animals↗

PubMed2006

Different plasma levels of vascular endothelial growth factor and nitric oxide between patients with choroidal and retinal neovascularization.

Because the blood flow is much more intense in the choroid than in the retina, it is interesting to explore whether choroidal neovascularization (CNV) is more influenced by plasma angiogenic factors than retinal neovascularization. The aim of this study was to investigate plasma profiles of vascular endothelial growth factor (VEGF) and nitric oxide (NO) in patients with CNV due to age-related macular degeneration (AMD) and in those with retinal neovascularization due to proliferative diabetic retinopathy (PDR). Seventy-seven subjects with AMD, 22 with PDR, and 42 nondiabetic, non-AMD controls were enrolled in this comparative case series. AMD subjects were classified into three groups: dry type (dry AMD, n = 17), wet type with active CNV (CNV/AMD, n = 42), and disciform scar due to advanced wet AMD (scar/AMD, n = 18). Plasma VEGF and NO levels of each subject were measured with enzyme-linked immunosorbent assay and chemiluminescence, respectively. Plasma VEGF level in CNV/AMD (median 256.0 pg/ml, interquartile range 146.4-375.3 pg/ml) was significantly higher than in PDR (124.8 pg/ml, 75.7-215.3 pg/ml; p = 0.004) and controls (120.3 pg/ml, 82.8-168.2 pg/ml, p =0.001). CNV/AMD also had the highest VEGF level among the AMD subgroups. Plasma NO level was significantly elevated in PDR (137.4 microM, 63.7-240.1 microM) when compared with CNV/AMD (71.8 microM, 42.4-113.3 microM; p = 0.004) and controls (62.6 microM, 39.0-114.9 microM; p = 0.002). There was no significant difference in NO levels among the AMD subgroups. No significant correlation between VEGF and NO levels was noted. These findings indicate that both circulating VEGF and NO may play different roles in the pathogenesis of retinal neovascularization and CNV.

Aged↗

PubMedDate not supplied

Role of vitronectin receptor-type integrins and osteopontin in ischemia-induced retinal neovascularization.

PURPOSE: It has been reported that vitronectin receptor-type integrins mediate vascular cell proliferation and migration. In this study, we investigated the expression of vitronectin receptor-type integrins and osteopontin in ischemia-induced retinal neovascularization, and examined the role of osteopontin in angiogenesis as a ligand of vitronectin receptor-type integrins. METHODS: Retinal neovascularization was produced by exposing C57BL/6J mice to 75% oxygen from postnatal day (P) 7 to P12. Expression of vitronectin receptor-type integrins and osteopontin was assessed by Northern blot analysis, in situ hybridization, and immunofluorescence. The role of osteopontin in retinal angiogenesis was evaluated by tube formation assay using cultured bovine retinal microcapillary endothelial cells. RESULTS: In the murine model, integrin alpha(v) mRNA was increased from P14 with a 2.6-fold peak response observed on P19, when retinal neovascularization was remarkable. Indirect immunofluorescence for vitronectin receptor-type integrins revealed prominent expression of integrin alpha(v)beta3/beta5 in the neovascular endothelial cells. Osteopontin mRNA was increased from P14, with a 2.0-fold peak response observed on P19. In situ hybridization demonstrated localization of osteopontin mRNA in neovascular tufts. Vascular endothelial growth factor-induced tube formation (8.3 +/- 0.6 mm/field) was inhibited significantly by treatment with anti-osteopontin antibody (4.8 +/- 0.7 mm/field, P <.001). CONCLUSIONS: These data suggest that increased expression of both vitronectin receptor-type integrins and osteopontin in ischemic retina contribute to vascular endothelial cell proliferation and to retinal vascular formation by promoting interaction between endothelial cells and extracellular matrix, which leads to retinal neovascularization.

Animals↗

PubMed1980

Studies on retinal neovascularization. Friedenwald Lecture.

Evidence supporting the original concept of Michaelson and Ashton of a vasoproliferative or angiogenesis factor responsible for retinal neovascularization is discussed. The oxygen model of retinal neovascularization is described as a key example in this evidence. Newer studies on experimental retinal neovascularization and its control are summarized.

Aged↗

PubMed2002

Immunolocalization and quantification of advanced glycation end products in retinal neovascular membranes and serum: a possible role in ocular neovascularization.

PURPOSE: Earlier studies have revealed the association of advanced glycation end products (AGE) with the pathogenesis of various micro and macro vascular complications. The purpose of the present study is to localize AGEs, namely carboxy methyl lysine (CML-AGE) and methyl glyoxal-derived AGEs (MG-AGE), in retinal neovascular membranes and to quantify them in serum samples. METHODS: Surgically excised retinal neovascular membranes and serum samples obtained from patients with diabetic retinopathy, Eales' disease and nondiabetics were studied. Immunolocalization of AGEs namely CML-AGE and MG-derived AGEs was done using avidin biotin complex method and quantification was done by enzyme linked immunosorbent assay (ELISA). RESULTS: CML-AGE immunoreactivity was detected in all cases of Eales' disease and 61% cases of diabetic retinopathy and none in idiopathic epiretinal membrane (ERM). MG-AGE immunoreactivity was observed in approximately 15% of diabetic retinopathy and none in Eales' disease and and idiopathic ERM. Quantification of AGEs in serum samples revealed statistically significant increased levels of MG-AGE in diabetes, in relation to nondiabetics with idiopathic ERM and CML-AGE in Eales' disease, in relation to diabetics and nondiabetics with idiopathic ERM. CONCLUSION: Results from this study suggest that AGEs formed through glycation and glycoxidation may play an important role in the development of retinal neovascularization. The immunoreactivity of CML-AGEs in neovascular membrane and its increased levels in serum suggest that inspite of the normoglycemic status, glycoxidation and lipid peroxidation due to oxidative stress may trigger retinal neovascularization in Eales' disease, while MG-AGEs in diabetic membrane and serum suggest the role of glycation. Thus the mechanism of neovascularization in different pathological conditions could be different.

Adolescent↗

PubMed2005

Bilateral sequential photodynamic therapy for sub-retinal neovascularization with type 2A parafoveal telangiectasis.

PURPOSE: To report the results of repeated bilateral sequential photodynamic therapy (PDT) with verteporfin for sub-retinal neovascularization associated with parafoveal telengiectasia. DESIGN: Interventional case series. METHODS: Three patients (minimum of 6-month follow-up) were analyzed after bilateral sequential PDT for parafoveal telengiectasia-associated sub-retinal neovascularization. RESULTS: Mean age was 53.3 +/- 2.1 years. Mean and median follow-up duration were 12.3 and 10 months, respectively. Mean initial Early Treatment of Diabetic Retinopathy Study chart letter acuity was 30.6 in right eyes and 19 in left eyes, and at month 6, it was 30.6 in right eyes and 22.3 in left eyes. All patients received bilateral treatment three times; one eye received a fourth treatment. The greatest linear diameter was between 2310 and 5400 microm. CONCLUSION: PDT is a viable treatment for sub-retinal neovascularization associated with parafoveal telengiectasia. Bilateral sequential treatment is a convenient way to treat bilateral disease.

Female↗

PubMed2006

Early vascular and neuronal changes in a VEGF transgenic mouse model of retinal neovascularization.

PURPOSE: To investigate early retinal changes in a vascular endothelial growth factor (VEGF) transgenic mouse (tr029VEGF; rhodopsin promoter) with long-term damage that mimics nonproliferative diabetic retinopathy (NPDR) and mild proliferative diabetic retinopathy (PDR). METHODS: Rhodopsin and VEGF expression was assessed up to postnatal day (P)28. Vascular and retinal changes were charted at P7 and P28 using sections and wholemounts stained with hematoxylin and eosin or isolectin IB4 Griffonia simplicifolia Samples were examined using light, fluorescence, and confocal microscopy. RESULTS: Rhodopsin was detected at P5 and reached mature levels by P15; VEGF protein expression was transient, peaking at P10 to P15. In wild-type (wt) mice at P7, vessels had formed in the nerve fiber/retinal ganglion cell layer and showed a centroperipheral maturational gradient; some capillaries had formed a second bed on the vitread side of the inner nuclear layer (INL). By P28, the retinal vasculature had three mature capillary beds, the third abutting the sclerad aspect of the INL. In tr029VEGF mice, capillary bed formation was accelerated compared with that in wt, with abnormal vessels extending to the sclerad side of the INL by P7 and abnormally penetrating the photoreceptors by P28. Compared with P7, vascular lesions were more numerous at P28 when capillary dropout was also evident. At both stages, retinal layers were thinned most where abnormal vessel growth was greatest. CONCLUSIONS: Concomitant damage to the vasculature and neural retina at early stages in tr029VEGF suggest that both tissues are affected, providing opportunities to examine early cellular events that lead to long-term disease.

Animals↗

PubMed2007

Role of nonproteolytically activated prorenin in pathologic, but not physiologic, retinal neovascularization.

PURPOSE: Recently, it was revealed that the inhibition of nonproteolytic activation of prorenin led to significant suppression of ocular inflammation in endotoxin-induced uveitis. The purpose of the present study was to investigate whether nonproteolytically activated prorenin plays a role in ischemia-induced retinal neovascularization. METHODS: C57BL/6 neonatal mice were reared in an 80% concentration of oxygen from postnatal (P) day 7 to P12, followed by room-air breathing to P17 to induce ischemia-initiated retinal neovascularization. Tissue localization of activated prorenin and prorenin receptor was examined by immunohistochemistry. Animals received intraperitoneal injections of handle-region peptide (HRP), a decoy peptide corresponding to the handle region of prorenin, which inhibits prorenin receptor-mediated upregulation of the renin-angiotensin system (RAS). A concanavalin A lectin perfusion-labeling technique was used to evaluate the areas of physiologic and pathologic retinal new vessels and the number of leukocytes adhering to the vasculature. Retinal mRNA expression and protein levels of intercellular adhesion molecule (ICAM)-1, vascular endothelial growth factor (VEGF), VEGF receptor (VEGFR)-1, and VEGFR-2 were examined by RT-PCR and ELISA. RESULTS: Retinal vessels in ischemic retinopathy eyes were positive for activated prorenin and prorenin receptor. Pathologic, but not physiologic, retinal neovascularization was significantly attenuated in HRP-treated mice compared with vehicle- or control peptide-treated animals. The number of adherent leukocytes was also significantly reduced. Retinal mRNA expression and protein levels of ICAM-1, VEGF, VEGFR-1, and VEGFR-2 in ischemic retinopathy were also significantly suppressed by the application of HRP. CONCLUSIONS: The present findings suggest that nonproteolytic activation of prorenin selectively promotes pathologic, but not physiologic, retinal neovascularization through the inflammatory processes related to pathologic neovascularization.

Animals↗