Andreas Stahl, Kip M Connor, Przemyslaw Sapieha, Jing Chen, Roberta J Dennison, Nathan M Krah, Molly R Seaward, Keirnan L Willett, Christopher M Aderman, Karen I Guerin, Jing Hua, Chatarina Löfqvist, Ann Hellström, Lois E H Smith. Invest Ophthalmol Vis Sci 2010
Times Cited: 410
Times Cited: 410
Times Cited
Times Co-cited
Similarity
Quantification of oxygen-induced retinopathy in the mouse: a model of vessel loss, vessel regrowth and pathological angiogenesis.
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Oxygen-induced retinopathy in the mouse.
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Dll4 signalling through Notch1 regulates formation of tip cells during angiogenesis.
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Ischemic neurons prevent vascular regeneration of neural tissue by secreting semaphorin 3A.
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Neurovascular crosstalk between interneurons and capillaries is required for vision.
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Characterization of retinal function and glial cell response in a mouse model of oxygen-induced retinopathy.
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Notch controls retinal blood vessel maturation and quiescence.
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Vascular endothelial growth factor-A is a survival factor for retinal neurons and a critical neuroprotectant during the adaptive response to ischemic injury.
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Neurons limit angiogenesis by titrating VEGF in retina.
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Proliferative retinopathies: angiogenesis that blinds.
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Effects of anti-VEGF treatment on the recovery of the developing retina following oxygen-induced retinopathy.
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Endothelial cells dynamically compete for the tip cell position during angiogenic sprouting.
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Ischemic Retinopathies: Oxidative Stress and Inflammation.
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Development of the hyaloid, choroidal and retinal vasculatures in the fetal human eye.
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The Notch ligand Delta-like 4 negatively regulates endothelial tip cell formation and vessel branching.
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