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Fight against angiogenesis-related blindness

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dc.contributor.authorJo, D.H.-
dc.contributor.authorKim, J.H.-
dc.date.accessioned2023-04-26T05:12:24Z-
dc.date.available2023-04-26T05:12:24Z-
dc.date.created2023-04-24-
dc.date.created2023-04-24-
dc.date.issued2012-
dc.identifier.citationRetinopathy: New Research, pp.79-92-
dc.identifier.urihttps://hdl.handle.net/10371/191640-
dc.description.abstractAngiogenesis-Related Blindness (ARB) indicates the spectrum of retinal diseases that can lead to catastrophic visual loss: retinopathy of prematurity in infants, retinoblastoma in children, diabetic retinopathy in the middle aged, and age-related macular degeneration in the elderly. These retinopathies are characterized by pathologic angiogenesis and breakdown of blood-retinal barrier (BRB) in common. With the evidences that vascular endothelial growth factor (VEGF) plays important role in angiogenesis and permeability, anti-VEGF treatment has been one of the mainstay modalities in managing ARB. However, there are limitations of anti-VEGF treatment in that it might not cure pathologic angiogenesis but induce decrease in differentiation or function of retinal neuronal cells. Recently, researches are in progress on modulation of upstream and downstream signaling molecules, in particular, HIF-1α and VEGF receptor-2, to suppress retinal and choroidal neovascularization. Furthermore, regulation of other angiogenic molecules and pathophysiologic mechanisms should be considered. We expect further researches on treatment of ARB to be more target-specific and pathogenesis-based. © 2012 Nova Science Publishers, Inc. All rights reserved.-
dc.language영어-
dc.publisherNova Science Publishers, Inc.-
dc.titleFight against angiogenesis-related blindness-
dc.typeArticle-
dc.citation.journaltitleRetinopathy: New Research-
dc.identifier.scopusid2-s2.0-84895223445-
dc.citation.endpage92-
dc.citation.startpage79-
dc.description.isOpenAccessN-
dc.contributor.affiliatedAuthorJo, D.H.-
dc.contributor.affiliatedAuthorKim, J.H.-
dc.type.docTypeBook Chapter-
dc.description.journalClass1-
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