Molekulare Mechanismen der Vaskulogenese und Angiogenese

Joussen, AM; Kirchhof, B.S.; Gottstein, Claudia

doi:10.1007/s00347-003-0799-x

Cited by 14 publications

(9 citation statements)

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“…In all these tissues of the anterior segment, bevacizumab is located preferably in the vessels walls (figs 1–3), which is the site of secretion and binding of VEGF to its receptors on the vascular endothelial cells 7. VEGF can be secreted by almost all cell types, including peri-endothelial cells 8. A certain concentration of VEGF is present in physiological vessel walls and acts as a survival factor for endothelial cells 9.…”

Section: Discussionmentioning

confidence: 99%

Immunohistochemical localisation of intravitreally injected bevacizumab in the anterior chamber angle, iris and ciliary body of the primate eye

Peters¹,

Heiduschka²,

Julien³

et al. 2008

British Journal of Ophthalmology

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Bevacizumab penetrates quickly into the iris, anterior chamber angle and ciliary body after intravitreal injection in the primate eye and accumulates particularly in blood-vessel walls. The highest concentration of bevacizumab in these tissues is present on day 1-4, the iris and anterior chamber angle being penetrated slightly earlier than the ciliary body. Our findings support the clinically observed rapid effect in the treatment of iris neovascularisation.

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Section: Discussionmentioning

confidence: 99%

Immunohistochemical localisation of intravitreally injected bevacizumab in the anterior chamber angle, iris and ciliary body of the primate eye

Peters¹,

Heiduschka²,

Julien³

et al. 2008

British Journal of Ophthalmology

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“…Although diabetic retinopathy is mainly characterized as a microvascular disease with concomitant lesions of the neuroretinal cells, there is much evidence that diabetic retinopathy is also an inflammatory disease [60,61,62]. As observed in ophthalmoscopic examination, diabetic retinopathy frequently presents with tissue destruction and attempts of tissue repair.…”

Section: Hypothetical Pathogenesis Of Pdvrmentioning

confidence: 99%

“…The third mechanism early in diabetic retinopathy by which hyperglycemia causes hypoxia is related to the leukocyte activation and adherence as leukocytes adhere to vascular endothelium. As Joussen et al [60,61,62] suggest, the inhibition of VEGF bioactivity may prove useful in the treatment of early diabetic retinopathy in the future[ 14]. …”

Section: Hypothetical Pathogenesis Of Pdvrmentioning

confidence: 99%

Pathogenesis and Classification of Proliferative Diabetic Vitreoretinopathy

Kroll¹,

Rodrigues²,

Hoerle³

2007

Ophthalmologica

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Purpose: To review the current knowledge regarding the pathogenesis of proliferative diabetic vitreoretinopathy (PDVR) and to present recommendations for its clinical staging. Design: Focused literature review and authors’ clinical experience. Results: Although several biochemical mediators may be responsible for the pathogenesis of PDVR, no common biochemical pathway exists. Of those mediators, vascular endothelial growth factor is the one most studied so far. However, since in proliferative diabetic retinopathy (PDR) the thickened posterior vitreous cortex is one of the main factors in the development of proliferations, a consequent shrinkage of the posterior vitreous cortex leads to hemorrhages and tractive retinal detachments. Therefore, PDR should be called PDVR. In consequence, the authors present a new morphological classification of PDVR. Conclusions: There is no consensus about the biochemical pathway responsible for the progression of PDVR. Although several classifications are described in the literature, the classification suggested here is important in the judgment of, the communication about and the therapy of diabetic retinopathy. Furthermore, it is the only reliable classification for predicting the surgical outcome in diabetics.

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“…Über einen komplexen, Rezeptor-Thyrosinkinase vermittelten Signalweg hat VEGF folgende Wirkungen: die Stimulation der Endothelzellproliferation, die Zunahme der vaskulären Permeabilität, ein chemotaktischer Effekt auf Makrophagen, der Erhalt von physiologischen Gefäßen [10,16]. Wird VEGF vom retinalen Pigmentepithel (RPE) überexprimiert, überwiegen proangiogenetische Faktoren, welches einen Stimulus für choroidale Neovaskularisationen darstellt [11,16,13]. Basierend auf dem pathophysiologischen Verständnis, dass VEGF einen zentralen Mediator der CNV-Induktion bei Patienten mit neovaskulärer AMD darstellt, wurden Anti-VEGF-Wirkstoffe entwickelt.…”

Section: Abstract !unclassified

Ranibizumab intravitreal zur Behandlung okkulter und klassischer choroidaler Neovaskularisation (CNV) bei AMD

Maier

Feucht²,

Fegert³

et al. 2010

Klin Monatsbl Augenheilkd

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Intravitreal application of Ranibizumab was safe and well tolerated. In the clinical situation, visual acuity was stabilised in the short term. As opposed to phase-III studies, no improvement in visual acuity could be accomplished. Cental retinal thickness decreased and findings in fluorescein angiography were stable within a 6-month follow-up period. It is necessary to perform monthly controls and proceed with VA- and OCT-based injections in order to maintain the therapeutic effect. Futher clinical evaluations of Ranibizumab will be necessary to evaluate its long-term treatment effects.

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Molekulare Mechanismen der Vaskulogenese und Angiogenese

Cited by 14 publications

References 0 publications

Immunohistochemical localisation of intravitreally injected bevacizumab in the anterior chamber angle, iris and ciliary body of the primate eye

Immunohistochemical localisation of intravitreally injected bevacizumab in the anterior chamber angle, iris and ciliary body of the primate eye

Pathogenesis and Classification of Proliferative Diabetic Vitreoretinopathy

Ranibizumab intravitreal zur Behandlung okkulter und klassischer choroidaler Neovaskularisation (CNV) bei AMD

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