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Soluble vascular endothelial growth factor receptor (VEGFR)-2 in macular oedema—a mechanism for regulating angiogenesis?
  1. Silvia Montoro-García1,2,
  2. Peck-Lin Lip3,
  3. Chi-Chao Chan4,
  4. Gregory Y H Lip1
  1. 1Haemostasis Thrombosis and Vascular Biology Unit, University of Birmingham Centre for Cardiovascular Sciences, City Hospital, Birmingham, UK
  2. 2Department of Cardiology, Hospital Universitario Virgen de la Arrixaca, Murcia, Spain
  3. 3Birmingham and Midland Eye Centre, Birmingham, UK
  4. 4National Eye Institute, National Institutes of Health, Bethesda, Maryland, USA
  1. Correspondence to Dr Gregory YH Lip, University of Birmingham Centre for Cardiovascular Sciences, City Hospital, Dudley Road, Birmingham B18 7QH, UK; g.y.h.lip{at}bham.ac.uk

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Central retinal vein occlusion (CRVO) is a common retinal condition and a major sight-threatening disease, where venous occlusion leads to a reduction in the oxygen supply to the retina, and subsequently, dysfunction of the blood–retinal barrier, chronic retinal hypoxia and increased retinal vascular permeability.1 All these pathophysiological processes lead to the development of impaired retinal vascular autoregulation and macular oedema, which may present as a slow deterioration of central visual function or as a high risk of neovascular glaucoma.2

Ischaemia is a major stimulus for angiogenesis, a biological response that leads to the formation of new blood vessels from existing vessels and induces aberrant development of retinal vessels into the vitreous. Angiogenesis is regulated, in part, by vascular endothelial growth factor (VEGF) and other vasoactive proteins such as angiopoietin. Thereby, changes in plasma VEGF and angiopoietin-2 levels in intraocular vascular remodelling have been investigated in retinal disease,3 as well as in atherosclerosis vascular disease4 and cancer metastasis.5 In the eye, hypoxia in the retinal periphery induces a fourfold upregulation of VEGF …

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