ライフサイエンスコーパス: retinal neovascularization

1 ascular endothelial growth factor (VEGF) and retinal neovascularization.

2 in the retinas of mice with hypoxia-induced retinal neovascularization.

3 nd dose-dependent deficiency of the expected retinal neovascularization.

4 pproach for ocular diseases characterized by retinal neovascularization.

5 oxygen (variable oxygen exposure) to induce retinal neovascularization.

6 n a dose-dependent manner, resulting in less retinal neovascularization.

7 ity, to examine the roles of MMP-2 and -9 in retinal neovascularization.

8 e an important factor in the pathogenesis of retinal neovascularization.

9 VEGF expression, in vivo in ischemia-induced retinal neovascularization.

10 ty and diabetic retinopathy are often due to retinal neovascularization.

11 signaling, suggesting a possible therapy for retinal neovascularization.

12 documented protein kinase CK2 involvement in retinal neovascularization.

13 hypothesis in a well-characterized model of retinal neovascularization.

14 for feedback inhibition of angiogenesis and retinal neovascularization.

15 H oxidase in causing VEGF overexpression and retinal neovascularization.

16 S-antigen-induced uveitis and laser-induced retinal neovascularization.

17 s, normalized VEGF expression, and prevented retinal neovascularization.

18 -stimulated increases in VEGF expression and retinal neovascularization.

19 and pStat3 was observed in association with retinal neovascularization.

20 n effective strategy for treating pathologic retinal neovascularization.

21 tion and VEGF production in a mouse model of retinal neovascularization.

22 tors in endothelial cells are protected from retinal neovascularization.

23 d to room air for 5 days (P12-P17) to induce retinal neovascularization.

24 ptor uPAR is essential to the development of retinal neovascularization.

25 ences between physiological and pathological retinal neovascularization.

26 ignal intermediates can significantly retard retinal neovascularization.

27 etinal vascular development and pathological retinal neovascularization.

28 in a significant reduction in the extent of retinal neovascularization.

29 ceptor (IGF-1R) are associated with abnormal retinal neovascularization.

30 ctions regulate the extent of oxygen-induced retinal neovascularization.

31 n-induced retinal ischemia without provoking retinal neovascularization.

32 ble NOS (iNOS) suppresses choroidal, but not retinal neovascularization.

33 f extracellular proteinase expression during retinal neovascularization.

34 enesis and discover novel drugs that inhibit retinal neovascularization.

35 Brown Norway (BN) rats with ischemia-induced retinal neovascularization.

36 a rat strain difference in susceptibility to retinal neovascularization.

37 itors of eNOS may be needed for treatment of retinal neovascularization.

38 s on P13 and P15, during the early stages of retinal neovascularization.

39 al endothelial cell growth and migration and retinal neovascularization.

40 d in the retina of experimental animals with retinal neovascularization.

41 lled and eyes enucleated for quantitation of retinal neovascularization.

42 ed in maintaining homeostasis and preventing retinal neovascularization.

43 e, or IPDX showed a significant reduction in retinal neovascularization.

44 ge role in diabetic maculapathy and diabetic retinal neovascularization.

45 tnatal days 7 through 12) was used to create retinal neovascularization.

46 field loss, vitrectomy, DME development, and retinal neovascularization.

47 s plays a permissive role in ischemia-driven retinal neovascularization.

48 xpression in tumors and during developmental retinal neovascularization.

49 paramount importance in the pathogenesis of retinal neovascularization.

50 tinopathy, they developed the same amount of retinal neovascularization.

51 nt and for ischemia-related tumor, iris, and retinal neovascularization.

52 GF2 in the retina affects the development of retinal neovascularization.

53 hyperoxia-induced retinopathy that exhibits retinal neovascularization.

54 pression are not likely to be complicated by retinal neovascularization.

55 essary nor sufficient for the development of retinal neovascularization.

56 w prospects for their therapeutic utility in retinal neovascularization.

57 ific deletion of GRP78 inhibited OIR-induced retinal neovascularization.

58 ggesting its involvement in ADAM10-regulated retinal neovascularization.

59 uced EC angiogenic responses and OIR-induced retinal neovascularization.

60 d the previously unexplored role of Ref-1 in retinal neovascularization.

61 o the ridge might similarly regress aberrant retinal neovascularization.

62 RORalpha substantially suppressed pathologic retinal neovascularization.

63 uced EC angiogenic responses and OIR-induced retinal neovascularization.

64 ition, intraocular injection of ManN induces retinal neovascularization.

65 duced Src-PLD1-PKCgamma-cPLA2 activation and retinal neovascularization.

66 duced Src-PLD1-PKCgamma-cPLA2 activation and retinal neovascularization.

67 al outcomes in rodent models of diabetes and retinal neovascularization.

68 d modulation of MEF2C may prevent pathologic retinal neovascularization.

69 proliferative diabetic retinopathy (PDR) is retinal neovascularization.

70 g its inhibitory effects on ischemia-induced retinal neovascularization.

71 ntrol is sufficient to achieve regression of retinal neovascularization.

72 e results in enhanced tumor angiogenesis and retinal neovascularization.

73 netic deletion suppressed both choroidal and retinal neovascularization.

74 LD1-PKCgamma signaling in retina, leading to retinal neovascularization.

75 FECH inhibitors could be repurposed to treat retinal neovascularization.

76 ion of PDGF-DD suppressed both choroidal and retinal neovascularization.

77 or mechanism by which omega3-PUFAs attenuate retinal neovascularization.

78 RNA approach also suppressed hypoxia-induced retinal neovascularization.

79 identify the genes and pathways involved in retinal neovascularization.

80 RAIL(-/-) mice had a significant increase in retinal neovascularization.

81 EGF-B targeting inhibited both choroidal and retinal neovascularization.

82 r obstruction (23%), retinal traction (20%), retinal neovascularization (6%), and retinal hole with d

83 ripheral nonperfusion (13/20 eyes, 65%), and retinal neovascularization (6/20 eyes, 30%).

84 ther species of PEDF significantly inhibited retinal neovascularization (83% for PEDF A and 55% for P

85 -up examinations showed shrinking of sea-fan retinal neovascularization, a complete resolution of ret

86 ischemic insult typically leads to aberrant retinal neovascularization, a major cause of blindness.

87 -FasL interaction plays an important role in retinal neovascularization after hyperoxia-induced injur

88 l tube formation in vitro and in vivo during retinal neovascularization after induction of VEGF expre

89 Eyes with initial retinal neovascularization all responded to the adjuvant

90 p.)-injected rBPI21 reduced ischemia-induced retinal neovascularization and diabetes-induced retinal

91 ction Fech(m1Pas) mutant mice showed reduced retinal neovascularization and endothelial cell prolifer

92 onditional knockout strain, but pathological retinal neovascularization and growth of heterotopically

93 cts developmental angiogenesis, pathological retinal neovascularization and heterotopic tumor growth.

94 c-abl is required for the hyperoxia-induced retinal neovascularization and hyperoxia-induced decreas

95 as a comprehensive resource for the study of retinal neovascularization and identification of potenti

96 Ischemia-induced hypoxia elicits retinal neovascularization and is a major component of s

97 ory effects of adiponectin overexpression on retinal neovascularization and leukocyte adhesion were a

98 suggest calcitriol is a potent inhibitor of retinal neovascularization and may be of benefit in the

99 exhibit critical features of MacTel such as retinal neovascularization and photoreceptor degeneratio

100 tion and chemical inhibition of Fech reduces retinal neovascularization and promotes physiological an

101 n explored as a therapy for various cancers, retinal neovascularization and pulmonary hypertension.

102 studies have shown that angiostatin inhibits retinal neovascularization and reduces retinal vascular

103 ly to be useful adjuncts in the treatment of retinal neovascularization and therapies designed to inc

104 d c-Met in the initiation and development of retinal neovascularization and to determine whether inhi

105 rference as a potential strategy to suppress retinal neovascularization and to prevent proliferative

106 lls and in a mouse model of ischemia-induced retinal neovascularization and to study the regulation o

107 are leading causes of vision loss evoked by retinal neovascularization and vascular leakage.

108 TM significantly inhibits retinal neovascularization and VEGF production in a mous

109 xynucleotides against murine VEGF to inhibit retinal neovascularization and VEGF synthesis in a murin

110 iogenesis is increased in some tissues (e.g. retinal neovascularization) and decreased in others (e.g

111 ecreased level of Matrigel plug and neonatal retinal neovascularization, and aortas isolated from Rap

112 cause of new blindness in young patients is retinal neovascularization, and in the elderly is choroi

113 le monitoring of the evolution of retinitis, retinal neovascularization, and other retinal changes.

114 is a rare disorder characterized by uveitis, retinal neovascularization, and retinal degeneration.

115 RORalpha is a novel regulator of pathologic retinal neovascularization, and RORalpha inhibition may

116 A6 peptide showed significant inhibition of retinal neovascularization, and the response was dose de

117 creased in a mouse model of ischemia-induced retinal neovascularization, and VEGF induced time- and d

118 ion is highly enhanced at the early stage of retinal neovascularization, and we found simultaneous re

119 Diseases characterized by retinal neovascularization are among the principal cause

120 rgeting pathological, but not physiological, retinal neovascularization are outlined.

121 hypoxia, VENIRKO mice show a 57% decrease in retinal neovascularization as compared with controls.

122 ression patterns in adult homeostasis and in retinal neovascularization associated with diabetes.

123 le human paradigm: spontaneous regression of retinal neovascularization associated with long-standing

124 d increased superoxide formation in areas of retinal neovascularization associated with relative reti

125 njection of 100 ng of digoxin at P12 reduced retinal neovascularization by >70% at P17.

126 ctin attenuated hypoxia-induced pathological retinal neovascularization by 35% in wild-type mice and

127 al administration of alpha-defensins reduced retinal neovascularization by 45% and 60%, respectively,

128 mRNA expression and significantly suppressed retinal neovascularization by approximately 40%.

129 nepafenac inhibits CNV and ischemia-induced retinal neovascularization by decreasing production of V

130 h CD13/APN inhibitors significantly impaired retinal neovascularization, chorioallantoic membrane ang

131 imals demonstrated a significant decrease in retinal neovascularization compared with control animals

132 hy (OIR) developed significantly less severe retinal neovascularization compared with wild-type (Wt)

133 but showed no difference in ischemia-induced retinal neovascularization compared with wild-type mice.

134 d no significant difference in the amount of retinal neovascularization compared with wild-type mice.

135 Retinal neovascularization decreased with increasing PAI

136 F therapy to prevent further vision loss and retinal neovascularization due to extensive retinal isch

137 optic disk demonstrate a higher incidence of retinal neovascularization due to heat-induced obstructi

138 o ischemia-induced retinopathy, pathological retinal neovascularization during ischemia was exacerbat

139 -2 in development of retinal vasculature and retinal neovascularization during oxygen-induced ischemi

140 ostnatal retinal vascularization, as well as retinal neovascularization during oxygen-induced ischemi

141 natal development of retinal vasculature and retinal neovascularization during oxygen-induced ischemi

142 mouse and human data indicate that reactive retinal neovascularization either fails to develop or re

143 hough chemical- and injury-induced models of retinal neovascularization exist, the need for a genetic

144 of CCN1 significantly decreases pathological retinal neovascularization following OIR.

145 tuation is more complex for ischemia-induced retinal neovascularization for which NO produced in endo

146 PPARgamma-mediated effect of omega3-PUFAs on retinal neovascularization formation and retinal angioge

147 by later vascular signs of DR, specifically retinal neovascularization, formation of new capillary b

148 vascular cells from tissues of patients with retinal neovascularization from PDR, we examined the eff

149 e presumed ocular histoplasmosis syndrome or retinal neovascularization from proliferative diabetic r

150 The association of retinal hypoxia with retinal neovascularization has been recognized for decad

151 ic nerve involvement, but the development of retinal neovascularization has been very rarely reported

152 Do agents that inhibit retinal neovascularization have any effect on choroidal

153 Retinal neovascularization impairs visual function and i

154 n of the NISAs RFE-007 and RFE-011 inhibited retinal neovascularization in a dose-dependent manner, c

155 fic inhibitors were tested for inhibition of retinal neovascularization in a mouse model of oxygen-in

156 16K hPRL inhibited retinal neovascularization in a mouse model of oxygen-in

157 to determine the effect of the ribozymes on retinal neovascularization in a mouse model of oxygen-in

158 (Pdeb(rd1)/Pdeb(rd1)) fail to mount reactive retinal neovascularization in a mouse model of oxygen-in

159 Captopril reduces retinal neovascularization in a mouse model of oxygen-in

160 eptor (EGFR) signaling, reduces pathological retinal neovascularization in a mouse model of oxygen-in

161 , was reported to protect against pathologic retinal neovascularization in a mouse model of oxygen-in

162 ic molecule, carboxyamido-triazole (CAI), on retinal neovascularization in a mouse model.

163 The extent of retinal neovascularization in a mouse OIR model was redu

164 iogenic inhibitor, inhibits ischemia-induced retinal neovascularization in a rat model.

165 We developed a novel model of retinal neovascularization in adult mice to examine the

166 AR interactions could suppress the extent of retinal neovascularization in an animal model of ischemi

167 re during normal development but had reduced retinal neovascularization in an OIR protocol.

168 Since VEGF is required for iris and retinal neovascularization in animal models of retinal i

169 dies have demonstrated partial inhibition of retinal neovascularization in animal models using antago

170 xia followed by normoxia induced significant retinal neovascularization in BN rats but not in SD rats

171 iogenesis may define new targets to suppress retinal neovascularization in diabetes and other ocular

172 ar, vessel loss resulting in hypoxia induces retinal neovascularization in diabetic retinopathy and i

173 se findings enable a pilot classification of retinal neovascularization in eyes with ROP using OCTA,

174 CAI almost completely abolished retinal neovascularization in group A, and neovascular f

175 or investigation and treatment of peripheral retinal neovascularization in her right eye(RE).

176 kage, edema, endothelial cell sprouting, and retinal neovascularization in ischemic retinas of mice e

177 ypoxia and is a major stimulatory factor for retinal neovascularization in ischemic retinopathies suc

178 VEGF-specific antagonists markedly suppress retinal neovascularization in mice and primates with isc

179 ibin expression cassette strongly suppressed retinal neovascularization in mice with ischemic retinop

180 eceptors (rho/VEGF mice) but did not inhibit retinal neovascularization in mice with ischemic retinop

181 study, we demonstrate complete inhibition of retinal neovascularization in mice with oxygen-induced i

182 mals, XMP.Z also suppressed ischemia-induced retinal neovascularization in mice.

183 previously described model of oxygen-induced retinal neovascularization in newborn mouse pups was use

184 le Ref-1 redox inhibitor, APX2009, decreased retinal neovascularization in OIR after systemic deliver

185 on of blocking antibodies to SDF-1 prevented retinal neovascularization in our murine model, even in

186 oncentrations, retinal vascular leakage, and retinal neovascularization in P17 mice subjected to oxyg

187 can impact the evaluation and management of retinal neovascularization in PDR.

188 beta 2 isoform and a significant decrease in retinal neovascularization in PKC beta isoform null mice

189 ntly decreases the formation of pathological retinal neovascularization in retinopathy.

190 rences in susceptibility to ischemia-induced retinal neovascularization in SD and BN rats.

191 ice to study the vascular flow in and around retinal neovascularization in seven preterm infants with

192 retinal inflammation, vascular leakage, and retinal neovascularization in the DR models.

193 how EC-specific ADAM10 regulates pathologic retinal neovascularization in the ischemic retina, indic

194 o be a useful tool for assessing the risk of retinal neovascularization in the newborn rat ROP model.

195 Arg-Gln dramatically inhibited retinal neovascularization in the OIR model.

196 ndothelial growth factor expression precedes retinal neovascularization in the retinas and the optic

197 gon laser in effecting lasting regression of retinal neovascularization in the setting of previously

198 s investigated by quantitating the extent of retinal neovascularization in the uPAR(-/-) mouse.

199 oroidal neovascularization and regression of retinal neovascularization in two models, transgenic mic

200 ve AdoR antagonists inhibited oxygen-induced retinal neovascularization in vivo and may provide a bas

201 show that alpha-defensins inhibit pathologic retinal neovascularization in vivo and may provide a cli

202 that an IGF-1 receptor antagonist suppresses retinal neovascularization in vivo, and infer that inter

203 , migration, and tube formation in vitro and retinal neovascularization in vivo.

204 endothelial capillary outgrowth in vitro and retinal neovascularization in vivo.

205 F-1 signaling are now shown to contribute to retinal neovascularization, in part, by modulating the e

206 f proteinases in the final common pathway of retinal neovascularization indicates that inhibition of

207 Isolated retinal neovascularization (IRNV) is a common finding in

208 Pathological retinal neovascularization is a cause of vision loss in

209 Proliferative retinopathy because of retinal neovascularization is a leading cause of blindne

210 Retinal neovascularization is a major cause of blindness

211 Pathologic retinal neovascularization is a potentially blinding con

212 Retinal neovascularization is one of the leading causes

213 Retinal neovascularization is the leading cause of visua

214 Retinal neovascularization is the major cause of untreat

215 e retinopathy, characterized by pathological retinal neovascularization, is a major cause of blindnes

216 In addition to retinal neovascularization, it involves retinal degenera

217 is a reproducible model of ischemia-induced retinal neovascularization; it is used commonly to devel

218 Cre mice display reduced angiogenesis in the retinal neovascularization model and in response to VEGF

219 cts of intravitreous bevacizumab in a rabbit retinal neovascularization model.

220 ,5,6,7-tetrabromobenzotriazole blocked mouse retinal neovascularization more efficiently than either

221 rrhage (n = 2), vitreous hemorrhage (n = 1), retinal neovascularization (n = 1), and cystoid macular

222 icated by the ICD-9-CM diagnosis of "362.16: Retinal Neovascularization NOS." RESULTS: The estimated

223 Clinical Modification diagnosis of "362.16: Retinal Neovascularization NOS." Type of initial treatme

224 eactivated plus disease; and 1 had recurrent retinal neovascularization not further specified).

225 The present study investigates whether retinal neovascularization (NV) and apoptosis are altere

226 ological inhibition of STING both alleviated retinal neovascularization (NV) and reduced retinal vasc

227 perimental retinopathy of prematurity (ROP), retinal neovascularization (NV) and vessel tortuosity ha

228 echanisms are implicated in the induction of retinal neovascularization (NV) during ischemic retinopa

229 ll types, the role of TRAIL in regulation of retinal neovascularization (NV) has not been described.

230 fect of administration of exogenous PAI-1 on retinal neovascularization (NV) in an animal model of re

231 n of mAbFzd7 or CRD significantly attenuated retinal neovascularization (NV) in mice with OIR.

232 tions of DXR or DNR suppressed choroidal and retinal neovascularization (NV), but also perturbed reti

233 growth factor (VEGF) has been implicated in retinal neovascularization (NV), but it has been difficu

234 ina triggers both normal vessel regrowth and retinal neovascularization (NV), which is maximal at P17

235 lecular imaging methods, to assess levels of retinal neovascularization (NV), would greatly benefit p

236 pout in early OIR and mitigated pathological retinal neovascularization (NV).

237 o investigate whether 12-LOX plays a role in retinal neovascularization (NV).

238 Changes in retinal neovascularization occur in the Nrl(-/-)Grk1(-/-

239 Retinal neovascularization occurring as a complication o

240 as a model for one of the variants of type 3 retinal neovascularization occurring in some patients wi

241 tinal detachment were increased if there was retinal neovascularization (odds ratio, 11.61; 95% CI, 1

242 2 in retinal photoreceptors but developed no retinal neovascularization or other abnormalities of ret

243 des did not cause a significant reduction in retinal neovascularization or VEGF protein levels.

244 s injected intraocularly in a mouse model of retinal neovascularization (oxygen-induced retinopathy [

245 ROP model showed a significant reduction in retinal neovascularization (P < 0.0001) and in the numbe

246 15 in rat) and to the later phase of maximum retinal neovascularization (P18 in mouse, P20 in rat) an

247 nhibition of the activity of uPAR suppresses retinal neovascularization, possibly through a reduction

248 or (TNF)-alpha as a regulator of MMPs in the retinal neovascularization process.

249 posure resulted in 78% and 82% inhibition of retinal neovascularization, respectively.

250 e efficiency for visualizing newly developed retinal neovascularization (RNV) and to monitor the dyna

251 tic target in the prevention or treatment of retinal neovascularization seen in many ocular diseases.

252 ssion with siRNA is effective in suppressing retinal neovascularization, suggesting EPO siRNA is a po

253 ffective for neuronal survival did not cause retinal neovascularization, suggesting that VEGF-B is th

254 etinal nonperfusion and little likelihood of retinal neovascularization suggests the possibility that

255 GF-1 signaling in endothelium play a role in retinal neovascularization through the expression of vas

256 tulated to be involved in the development of retinal neovascularization through the regulation of ext

257 CTGF/CCN2 stimulates retinal neovascularization through transactivation of p5

258 Our results demonstrate human retinal neovascularization, thus revealing the functiona

259 d a novel mouse xenotransplantation model of retinal neovascularization to test human hematopoietic c

260 atic steroid, anecortave acetate, to inhibit retinal neovascularization using a rat model of ROP and

261 Is it possible to completely inhibit retinal neovascularization using drug treatment with a m

262 into ischemic retina and strongly suppressed retinal neovascularization, VEGF-induced subretinal neov

263 duced Src-PLD1-PKCgamma-cPLA2 activation and retinal neovascularization via activation of Kdr and Flt

264 icant reduction in vascular obliteration and retinal neovascularization vs. saline injection in the O

265 Cs), and the mouse model of ischemia-induced retinal neovascularization was assayed by real-time PCR

266 In addition, retinal neovascularization was assessed by quantificatio

267 In addition, retinal neovascularization was attenuated in PECAM-1-/-

268 the oxygen-induced ROP neonatal mouse model, retinal neovascularization was decreased by 40% +/- 16%

269 Oxygen-induced retinal neovascularization was established in neonatal m

270 Retinal neovascularization was evaluated using flatmount

271 Retinal neovascularization was evaluated using fluoresce

272 Retinal neovascularization was examined by fluorescein d

273 f AdoR antagonist administration in reducing retinal neovascularization was examined in a mouse pup m

274 Additional retinal neovascularization was found in 1 patient.

275 Retinal neovascularization was induced by exposing newbo

276 Retinal neovascularization was induced in mice pups by e

277 Abnormal retinal neovascularization was induced in rat pups by su

278 Retinal neovascularization was inhibited in these mice i

279 Stat3 in the mouse model of ischemia-induced retinal neovascularization was investigated to evaluate

280 ficant reduction in the severity of abnormal retinal neovascularization was observed in the steroid-t

281 Hyperoxia-induced retinal neovascularization was observed in wild-type and

282 Retinal neovascularization was present bilaterally in 2

283 Retinal neovascularization was scored, and avascular are

284 This effect was dose dependent, and retinal neovascularization was significantly inhibited i

285 However, the degree of ischemia-induced retinal neovascularization was significantly reduced in

286 f growth hormone (GH) in ischemia-associated retinal neovascularization was studied in transgenic mic

287 l neovascular specimens and rodent models of retinal neovascularization, we discovered that pathologi

288 n understanding the mechanisms of pathologic retinal neovascularization, we found that VEGF activates

289 In view of understanding the mechanisms of retinal neovascularization, we had reported previously t

290 Retinal vascular area and retinal neovascularization were assessed by adenosine di

291 Children with intraocular surgery or active retinal neovascularization were excluded from the study.

292 e uPA/uPAR interaction on the development of retinal neovascularization were studied in this animal m

293 n from injured eyes caused a 60% decrease in retinal neovascularization when injected into the vitreo

294 uced retinal vascular leakage and attenuated retinal neovascularization, when compared with the contr

295 But FECH has not been explored in retinal neovascularization, which underlies diseases lik

296 Parstatin suppressed retinal neovascularization with maximum inhibition of 60

297 rickettsial retinitis may develop a sea-fan retinal neovascularization, with subsequent vitreous hem

298 jection of VEGF in rabbits results in florid retinal neovascularization within the first week, follow

299 nal VEGF expression and reduces pathological retinal neovascularization without obvious side effects.

300 oss and consequent hypoxia-driven pathologic retinal neovascularization, yet relatively little is kno