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Marmor, Michael F.

doi:10.1023/a:1002192829817

Cited by 222 publications

(54 citation statements)

References 7 publications

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“…The outer retinal layers appeared to be the privileged site for tissue swelling which is consistent with previous findings [6,28]. In our study, cystoid DME was present in 54.2% of the 59 eyes, the majority (52 eyes; 88.1%) involving the outer retinal layers - outer cystoid DME (type 3).…”

Section: Resultssupporting

confidence: 92%

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Degree of Decrease in Central Retinal Thickness Predicts Visual Acuity Response to Intravitreal Ranibizumab in Diabetic Macular Edema

Santos

Gomes

Figueira³

et al. 2013

Ophthalmologica

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Purpose: To characterize factors that may be associated with optimal or suboptimal response to ranibizumab intravitreal injections in diabetic macular edema (DME). Methods: Fifty-nine eyes with DME treated with ranibizumab were included. All underwent best-corrected visual acuity (BCVA) assessment and optical coherence tomography (OCT) at baseline, 3 and 6 months. Central retinal thickness (CRT) was assessed at each visit, and OCT images were classified according to their morphological patterns. Results: A mean BCVA increase of 4.78 and 5.52 letters, and a CRT decrease of 80.25 and 106.12 µm were found after 3 and 6 months of treatment (p < 0.001). BCVA improvement was found to be dependent on baseline BCVA and the degree of CRT decrease. Twenty-six eyes (44%) showing a CRT decrease ≥20% improved BCVA by 10.3 ± 13.0 letters, whereas 33 eyes (56%) with a CRT decrease <20% had BCVA improvement of 1.8 ± 7.2 letters (odds ratio = 3.31). Conclusions: The degree of CRT decrease obtained by spectral-domain OCT identifies well the optimal responders to intravitreal ranibizumab and predicts BCVA improvement after treatment.

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Section: Resultssupporting

confidence: 92%

“…The resulting increase in the vascular permeability leads to accumulation of fluid and proteins on the macula causing DME [3,4,5,6]. Anti-VEGF drugs, such as ranibizumab, have shown their efficacy in treating DME.…”

Section: Introductionmentioning

confidence: 99%

Degree of Decrease in Central Retinal Thickness Predicts Visual Acuity Response to Intravitreal Ranibizumab in Diabetic Macular Edema

Santos

Gomes

Figueira³

et al. 2013

Ophthalmologica

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“…Although the excessive fluid mainly comes from capillaries in the inner retina, the removal of subretinal fluid is dependent on the RPE. The maintenance of RPE barrier function is essential for the efficient removal of the fluid (3), and the disruption of the RPE barrier can eventually lead to choroidal neovascularization.…”

Section: Age-related Macular Degeneration (Amd)mentioning

confidence: 99%

Pigment Epithelium-derived Factor Maintains Retinal Pigment Epithelium Function by Inhibiting Vascular Endothelial Growth Factor-R2 Signaling through γ-Secretase

Ablonczy

Prakasam

Fant

et al. 2009

Journal of Biological Chemistry

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Wet age-related macular degeneration (AMD) attacks the integrity of the retinal pigment epithelium (RPE) barrier system. The pathogenic process was hypothesized to be mediated by vascular endothelial growth factor (VEGF) and antagonized by pigment epithelium-derived factor (PEDF). To dissect these functional interactions, monolayer cultures of RPE cells were established, and changes in transepithelial resistance were evaluated after administration of PEDF, placenta growth factor (VEGF-R1 agonist), and VEGF-E (VEGF-R2 agonist). A recently described mechanism of VEGF inhibition in endothelia required the release of VEGF-R1 intracellular domain by ␥-secretase. To evaluate this pathway in the RPE, cells were pretreated with inhibitors DAPT or LY411575. Processing of VEGF receptors was assessed by Western blot analysis. Administration of VEGF-E rapidly increased RPE permeability, and PEDF inhibited the VEGF-E response dose-dependently. Both ␥-secretase antagonists prevented the inhibitory effects of PEDF. The co-administration of PEDF and VEGF-E depleted the amount of VEGF-R2 in the membrane and increased the amount of VEGF-R2 ectodomain in the media. Therefore, the inhibitory effect of PEDF appears to be mediated via the processing of VEGF-R2 by ␥-secretase. ␥-Secretase generates the amyloid-␤ (A␤) peptide of Alzheimer disease from its precursor (amyloid precursor protein). This peptide is also a component of drusen in dry AMD. The results support the hypothesis that misregulation of ␥-secretase may not only lead to A␤ deposits in dry AMD but can also be damaging to RPE function by blocking the protective effects of PEDF to prevent VEGF from driving the dry to wet AMD transition. Age-related macular degeneration (AMD)2 is often diagnosed by the appearance of subretinal fluid. This fluid causes a local detachment of the retina in the macular area resulting in decreased visual acuity in the center of the visual field (1). The resulting macular edema can lead to complete vision loss (2). Although the excessive fluid mainly comes from capillaries in the inner retina, the removal of subretinal fluid is dependent on the RPE. The maintenance of RPE barrier function is essential for the efficient removal of the fluid (3), and the disruption of the RPE barrier can eventually lead to choroidal neovascularization.Recent clinical studies have shown that intravitreally administered anti-VEGF compounds are effective therapies for choroidal neovascularization (4 -6). Originally, VEGF was described as an endothelial angiogenic and vasopermeability factor. The leakage through the vessels of the inner retina increases in response to VEGF (7,8). However, the release of VEGF also affects RPE function (9 -11). We have recently shown that RPE barrier integrity is modulated by VEGF through apically oriented VEGF-R2 receptors (12). Thus, there is a growing body of evidence that intraocular VEGF can increase the permeability of both the inner and outer bloodretina barriers, contributing to the accumulation of subretinal fluid and macular ed...

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“…Macular edema represents the common final pathway of many intraocular and systemic diseases as a nonspecific sign usually involving the retinal vessels [1,2]. While the progression of symptoms is usually slow, patients may still experience a sudden onset, depending on the etiology.…”

Section: Introductionmentioning

confidence: 99%

Pathophysiology of Macular Edema

Scholl¹,

2010

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Macular edema is defined as an accumulation of fluid in the outer plexiform layer and the inner nuclear layer as well as a swelling of Müller cells of the retina. It consists of a localized expansion of the retinal extracellular space (sometimes associated with the intracellular space) in the macular area. Macular edema is a common cause of a sudden or chronic decrease in visual acuity occurring in many ocular diseases such as age-related macular degeneration, diabetic retinopathy and retinal vein occlusion. As a nonspecific sign of many intraocular and systemic diseases, macular edema represents a common final pathway. The existence of the blood-retinal barrier (BRB) formed by intercellular junctions is the precondition required to maintain this physiological status. This status may become severely disturbed by many diseases, finally resulting in macular edema. In this article, the development of macular edema will also be classified by its pathophysiological and pathobiochemical pathways. Vascular components, the dysfunctional BRB, the role of proteins and water fluxes as well as the role of several inflammatory mediators (e.g. angiotensin II, vascular endothelial growth factor, prostaglandins) in the retina will be discussed as responsible mechanisms leading to the development of macular edema.

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Untitled

Cited by 222 publications

References 7 publications

Degree of Decrease in Central Retinal Thickness Predicts Visual Acuity Response to Intravitreal Ranibizumab in Diabetic Macular Edema

Degree of Decrease in Central Retinal Thickness Predicts Visual Acuity Response to Intravitreal Ranibizumab in Diabetic Macular Edema

Pigment Epithelium-derived Factor Maintains Retinal Pigment Epithelium Function by Inhibiting Vascular Endothelial Growth Factor-R2 Signaling through γ-Secretase

Pathophysiology of Macular Edema

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