Angiotensin II and vascular endothelial growth factor in the vitreous fluid of patients with diabetic macular edema and other retinal disorders

Funatsu, Hideharu; Yamashita, Hidetoshi; Ikeda, Tomohiro; Nakanishi, Yuichiro; Kitano, Shigehiko; Hori, Shingo

doi:10.1016/s0002-9394(02)01323-5

Cited by 157 publications

(99 citation statements)

References 31 publications

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“…118 Vitreous levels of several inflammatory cytokines (including IL-6, IL-8, and monocyte chemotactic protein (MCP)-1) are increased in eyes with DMO and PDR. 119 In other studies, Funatsu et al [120][121][122] have reported significant elevations of VEGF, ICAM-1, IL-6, MCP-1, and pigment epithelium-derived factor, which correlated with retinal vascular permeability changes. In addition to this pathway, stimulation of 6-N-acetyl glucosaminyl-transferase in leukocyte can result in more modification of glycans on its surface thus inducing leukocyte rolling interactions to endothelial selectins.…”

Section: Scientific Basismentioning

confidence: 89%

“…The elevated cytokines include VEGF, MCP-1, IL-6, IL-8, interferon γ-induced protein-10. 119,130-132 Funatsu et al [120][121][122] have also previously reported increased levels of ICAM-1, IL-6, Angiotensin II, and VEGF in DR and DMO. Klein et al 133 reported that sVCAM-1 and TNFα are associated with higher odds of developing more severe DR in patients with renal disease and PDR.…”

Section: Scientific Basismentioning

confidence: 91%

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A review of therapies for diabetic macular oedema and rationale for combination therapy

Amoaku

Saker

Stewart

2015

Eye

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Diabetic macular oedema (DMO) is responsible for significant visual impairment in diabetic patients. The primary cause of DMO is fluid leakage resulting from increased vascular permeability through contributory anatomical and biochemical changes. These include endothelial cell (EC) death or dysfunction, pericyte loss or dysfunction, thickened basement membrane, loss or dysfunction of glial cells, and loss/change of EC Glycocalyx. The molecular changes include increased reactive oxygen species, pro-inflammatory changes: advanced glycation end products, intracellular adhesion molecule-1, Complement 5-9 deposition and cytokines, which result in increased paracellular permeability, tight junction disruption, and increased transcellular permeability. Laser photocoagulation has been the mainstay of treatment until recently when pharmacological treatments were introduced. The current treatments for DMO target reducing vascular leak in the macula once it has occurred, they do not attempt to treat the underlying pathology. These pharmacological treatments are aimed at antagonising vascular endothelial growth factor (VEGF) or non-VEGF inflammatory pathways, and include intravitreal injections of anti-VEGFs (ranibizumab, aflibercept or bevacizumab) or steroids (fluocinolone, dexamethasone or triamcinolone) as single therapies. The available evidence suggests that each individual treatment modality in DMO does not result in a completely dry macula in most cases. The ideal treatment for DMO should improve vision and improve morphological changes in the macular (eg, reduce macular oedema) for a significant duration, reduced adverse events, reduced treatment burden and costs, and be well tolerated by patients. This review evaluates the individual treatments available as monotherapies, and discusses the rationale and potential for combination therapy in DMO.

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Section: Scientific Basismentioning

confidence: 89%

Section: Scientific Basismentioning

confidence: 91%

A review of therapies for diabetic macular oedema and rationale for combination therapy

Amoaku

Saker

Stewart

2015

Eye

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“…Aqueous humor, in patients with neovascular AMD, contained elevated concentrations of vascular endothelial growth factor (VEGF) and angiogenin, as well as specific cytokines (IP-10, Mig MIP-1β and MCP-1) [19]. VEGF and interleukin-6 (IL-6) is also present in the aqueous humor in patients with diabetic retinopathy [20,21].…”

Section: Introductionmentioning

confidence: 99%

Gap Junction Coupled Cells, Barriers and Systemic Inflammation

Rönnbäck¹

2017

IJOAO

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The blood-brain barrier (BBB), the blood-retinal barrier (BRB), and the blood-nerve barrier (BNB) may have similarities in systemic chronic inflammation, as seen in a variety of diseases. A disturbance of the barriers lead to a disruption of the cells coupled with gap junctions in syncytium. The network coupling may be principal to understand the homeostatic imbalance in systemic inflammation. This review high-lightens the role of gap junction network coupled cells in inducing and maintaining barrier properties under physiological conditions as well as their involvement in inflammatory pathologies. Rigshospitalet, 2600 Glostrup, Denmark, Tel. +45 3863 4820, Fax +45 3863 4834; E-mail elisabeth.cecilia.roennbaeck@regionh.dk and waste products between the vascular lumen and the neural retina and is formed by the interaction of retinal glia and pericytes with the endothelium. The blood-nerve barrier (BNB) consists of blood vessels and sensory nerves but gap junction coupled cells in networks, such as the articular cartilage in joints, might be involved in these cell interactions [3]. KeywordsFuture studies elucidating barrier induction and maintenance will provide a framework for rational therapies in several diseases, to restore the barriers with influence of gap junction syncytium coupled cells on the barrier functions.

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“…6 Increased levels of angiotensin II in the vitreous, and of interleukin-6 and vascular endothelial growth factor in the aqueous humour and plasma, have also been associated with DME. 7,8 The Early Treatment Diabetic Retinopathy Study Research Group showed that, in eyes with DME, focal laser photocoagulation reduces the risk of moderate visual loss by 50% or more, decreases the frequency of persistent macular oedema, and increases the chance for improvement in best-corrected visual acuity (BCVA). However, 15% of eyes experienced moderate visual loss after 3 years of followup despite focal laser photocoagulation.…”

Section: Introductionmentioning

confidence: 99%

Diabetic vitreopapillary traction and macular oedema

Karataş

Ramírez

Ophir

2004

Eye

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Purpose To describe an association between optic disc traction and diabetic macular oedema (DME) unresponsive to laser treatment. Methods A retrospective review of all patients with DME who attended our clinic between September 2001 and November 2003 was undertaken. The patients had undergone ophthalmic history and examination, fluorescein angiography, and optical coherence tomography (OCT) of the macular area and optic nerve head (ONH). A total of 10 nonvitrectomized eyes that were found to have an elevation of the ONH secondary to vitreopapillary traction were included in the analysis. Eyes with additional traction at the posterior pole were excluded. Results Out of the 10 eyes (seven patients, aged 47-79 years) with vitreo-papillary traction, nine had previously undergone argon laser photocoagulation(s) for DME. In seven eyes (seven patients), OCT verified the vitreopapillary traction as the sole traction, whereas in the fellow eyes of three patients vitreomacular traction was evident as well. In the seven eyes with only vitreopapillary traction, OCT demonstrated parapapillary serous retinal detachment in two eyes and a diffuse DME in all eyes (mean foveal thickness, 3967144 lm). Maximal thickness of the papillo-macular bundle site was adjoining the elevated ONH in three eyes, and was maximal at the central macula in the other four eyes. Ultrasonography (n ¼ 5) revealed an incomplete detachment of the posterior hyaloid in each, adherent only at the ONH. Conclusions Diffuse DME unresponsive to laser treatment may be associated with vitreopapillary traction. Further studies should indicate whether these two phenomena could suggest a cause and effect in such eyes.

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Angiotensin II and vascular endothelial growth factor in the vitreous fluid of patients with diabetic macular edema and other retinal disorders

Cited by 157 publications

References 31 publications

A review of therapies for diabetic macular oedema and rationale for combination therapy

A review of therapies for diabetic macular oedema and rationale for combination therapy

Gap Junction Coupled Cells, Barriers and Systemic Inflammation

Diabetic vitreopapillary traction and macular oedema

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