Ocular Neovascularization: Basic Mechanisms and Therapeutic Advances

Dorrell, Michael I.; Uusitalo‐Järvinen, Hannele; Aguilar, Edith; Friedlander, Martin

doi:10.1016/j.survophthal.2006.10.017

Cited by 121 publications

(96 citation statements)

References 179 publications

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“…As in other ocular pathologies, such as diabetic retinopathy and age-related macular degeneration (AMD), vision loss is the result of aberrant neoangiogenesis caused by overexpression of the proangiogenic factor VEGF (3)(4)(5). ROP is a biphasic disease consisting of an initial phase of hyperoxia that induces irreversible damage to immature retinal vessels of the neonate, resulting in retinal ischemia, followed by a second phase of hypoxia-induced pathological neoangiogenesis.…”

mentioning

confidence: 99%

Genetic and pharmacological inhibition of JNK ameliorates hypoxia-induced retinopathy through interference with VEGF expression

Gumá

Rius

Duong-Polk

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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Many ocular pathologies, including retinopathy of prematurity (ROP), diabetic retinopathy, and age-related macular degeneration, result in vision loss because of aberrant neoangiogenesis. A common feature of these conditions is the presence of hypoxic areas and overexpression of the proangiogenic vascular endothelial growth factor (VEGF). The prevailing current treatment, laser ablation of the retina, is destructive and only partially effective. Preventive and less destructive therapies are much more desirable. Here, we show that mice lacking c-Jun N-terminal kinase 1 (JNK1) exhibit reduced pathological angiogenesis and lower levels of retinal VEGF production in a murine model of ROP. We found that hypoxia induces JNK activation and regulates VEGF expression by enhancing the binding of phospho-c-Jun to the VEGF promoter. Intravitreal injection of a specific JNK inhibitor decreases retinal VEGF expression and reduces pathological retinal neovascularization without obvious side effects. These results strongly suggest that JNK1 plays a key role in retinal neoangiogenesis and that it represents a new pharmacological target for treatment of diseases where excessive neoangiogenesis is the underlying pathology.neoangiogenesis ͉ retinopathy of prematurity

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mentioning

confidence: 99%

Genetic and pharmacological inhibition of JNK ameliorates hypoxia-induced retinopathy through interference with VEGF expression

Gumá

Rius

Duong-Polk

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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“…Like the brain, the postnatal retina is also initially avascular and invaded by vascular sprouts from the optic nerve, a process that occurs during the first two postnatal weeks in mice (Dorrell et al 2007). VEGF produced by hypoxic retinal astrocytes leads to tip cell migration via VEGFR2 .…”

Section: Development and Maturation Of Cns Vesselsmentioning

confidence: 99%

Molecular Parallels between Neural and Vascular Development

Eichmann

Thomas

2012

Cold Spring Harbor Perspectives in Medicine

110

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The human central nervous system (CNS) features a network of 400 miles of blood vessels that receives .20% of the body's cardiac output and uses most of its blood glucose. Many human diseases, including stroke, retinopathy, and cancer, are associated with the biology of CNS blood vessels. These vessels originate from extrinsic cell populations, including endothelial cells and pericytes that colonize the CNS and interact with glia and neurons to establish the blood -brain barrier and control cerebrovascular exchanges. Neurovascular interactions also play important roles in adult neurogenic niches, which harbor a unique population of neural stem cells that are intimately associated with blood vessels. We here review the cellular and molecular mechanisms required to establish the CNS vascular network, with a special focus on neurovascular interactions and the functions of vascular endothelial growth factors.

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“…9,10 Vasculogenesis is seen predominantly during embryogenesis, whereas angiogenesis occurs also in adults in the context of wound healing, pregnancy, and uterine cycling. 11 However, angiogenesis has also been found to have a major role in pathological processes such as tumour growth and metastasis, as well as ocular neovascularisation (Figure 1). 10,12 Mechanisms and mediators of pathologic angiogenesis are thought to differ somewhat from physiological angiogenesis, exemplified by the fact that the latter does not usually carry an inflammatory component.…”

Section: Vascular Growth During Development Entails Vasculogenesis Anmentioning

confidence: 99%

Emerging techniques to treat corneal neovascularisation

Menzel‐Severing

2011

Eye

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Neovascularisation is a major cause of visual loss in a number of ophthalmic diseases. This review aims to outline the basic regulators of vessel growth in corneal neovascularisation. An understanding of the underlying principles of physiological and pathophysiological vascular development helps to appreciate current approaches to prevent or treat corneal neovascularisation. Options for future interventions will be discussed in the light of recent evidence provided by animal models of corneal neovascularisation.

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Ocular Neovascularization: Basic Mechanisms and Therapeutic Advances

Cited by 121 publications

References 179 publications

Genetic and pharmacological inhibition of JNK ameliorates hypoxia-induced retinopathy through interference with VEGF expression

Genetic and pharmacological inhibition of JNK ameliorates hypoxia-induced retinopathy through interference with VEGF expression

Molecular Parallels between Neural and Vascular Development

Emerging techniques to treat corneal neovascularisation

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