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• W2081001908 abstract "In the recent prospective randomized clinical trial, regular anti-VEGF treatment significantly increased best corrected visual acuity and decreased macular oedema in patients with central retinal vein occlusion (CRVO) compared with those who had a sham treatment (Epstein et al. 2012). Based on these data, intravitreal injections of anti-VEGF agents are now emerging as a part of the first-line treatment for CRVO. However, the VEGF blockade in the retina might have detrimental long-term local side effects (Kurihara et al. 2012). Therefore, development of alternative treatment modalities for CRVO remains a priority. In contrast to VEGF, the role of another potent vasoactive factor, angiopoietin (Ang)-2, is unknown in the pathogenesis of ischaemic CRVO. Angiopoietins are endothelial cell (EC)-specific growth factors essential for vascular integrity and remodelling. Ang-2 is almost exclusively produced and secreted by activated EC Weibel–Palade bodies during mechanical vascular wall injury, ischaemia and inflammation. Ang-2 has context-dependent agonist or antagonist effects on Tie2 receptor and controls vascular stabilization, EC and pericyte survival, and neovascularization in concert with the VEGF/VEGF-receptor system. Ang-2 expression correlates with ischaemic retinal neovascularization and has been found essential in making retinal vessels sensitive to the effects of intravitreous adenoviral VEGF gene transfer. Administration of Ang-2 blocking antibodies improved endothelial stability and inhibited retinal and choroidal neovascularization with similar efficacy as anti-VEGF antibodies (Rennel et al. 2011). Several studies have shown that the simultaneous blockade of Ang-2/Tie2 and VEGF pathways reduces vascular leakage and tumour sprouting angiogenesis and has an additive effect to single-agent treatment without apparent increased systemic toxicity (Koh et al. 2010). Combined inhibition of Tie-2 and VEGF signalling was also more effective in terminating pathological retinal neovascularization than anti-VEGF therapy alone (Takagi et al. 2003). In this study, we performed vitrectomy for the management of sight-threatening complications of ischaemic RVO in four patients (Table 1). Vitreous haemorrhage, neovascularization and some fibrosis formation were observed in all RVO eyes. None of the patients had previous ophthalmologic history or diabetes prior to RVO. Intravitreal injections of anti-VEGF blockade, such as with bevacizumab or ranibizumab, were not used in any of the study eyes preoperatively. The intravitreal concentrations of both Ang-2 and VEGF were significantly higher in eyes undergoing primary vitrectomy due to complicated RVO compared with eyes with a quiescent idiopathic macular hole or pucker (p 0.001; Table 1). This observation, together with the finding of normal intravitreal total protein and plasma Ang-2 levels among the patients with RVO, suggests that ischaemic retinal ECs secrete more Ang-2 than arises due to leakage from blood as a result of blood–retinal barrier breakdown. Interestingly, Ang-1, a factor with known vasculoprotective properties, was induced in RVO eyes. Based on these findings, we suggest that the combination of Ang-2 inhibitors with anti-VEGF therapy may be a more potent treatment for RVO than anti-VEGF therapy alone. However, clinical trials are needed to confirm our hypothesis. This study was supported by grants from the Finnish Eye Foundation, the Eye and Tissue Bank Foundation, the Mary and Georg C. Ehrnrooth Foundation, the Nissi Foundation, and HUCH Clinical Research Grants (TKK4150 and TYH1325)." @default.
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• W2081001908 date "2013-06-21" @default.
• W2081001908 modified "2023-09-27" @default.
• W2081001908 title "Increased intravitreal angiopoietin‐2 levels in patients with retinal vein occlusion" @default.
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• W2081001908 doi "https://doi.org/10.1111/aos.12223" @default.
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