The Role of Inflammation in the Pathogenesis of Glaucoma

Vohra, Rupali; Tsai, James C.; Kolko, Miriam

doi:10.1016/j.survophthal.2012.08.010

Cited by 188 publications

(164 citation statements)

References 79 publications

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“…Calciumdependent zinc endopeptidases known as MMPs degrade and remodulate the extracellular matrix in different tissues. During neurodegeneration MMPs seem to have important roles, so far only studied in some diseases for example glaucoma, where genes associated with cytokines and TNF-α in glial cells are upregulated and a low-grade inflammation may play a crucial role [49]. In glaucoma, a degeneration of retinal ganglion cells and retinal nerve fibers are seen and an up-regulation of MMP-2, -9, and -13 have been observed [50].…”

Section: Diseases Involved In Barrier Disruptionmentioning

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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Section: Diseases Involved In Barrier Disruptionmentioning

confidence: 99%

Gap Junction Coupled Cells, Barriers and Systemic Inflammation

Rönnbäck¹

2017

IJOAO

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“…Several studies focusing on the role of microglial cells in glaucoma have shown that these cells have alterations in morphology, gene expression, cell proliferation, cell adhesion, and immune response, compatible with a reactive phenotype [89,[97][98][99][100][101]. In fact, growing evidence demonstrates that the interactions between RGCs and glia are critically important for glaucomatous neurodegeneration [98,[102][103][104].…”

Section: Glaucomamentioning

confidence: 99%

Contribution of microglia‐mediated neuroinflammation to retinal degenerative diseases

Boia

Madeira

Aires

et al. 2017

Acta Ophthalmologica

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Retinal degenerative diseases are major causes of vision loss and blindness worldwide and are characterized by chronic and progressive neuronal loss. One common feature of retinal degenerative diseases and brain neurodegenerative diseases is chronic neuroinflammation. There is growing evidence that retinal microglia, as in the brain, become activated in the course of retinal degenerative diseases, having a pivotal role in the initiation and propagation of the neurodegenerative process. A better understanding of the events elicited and mediated by retinal microglia will contribute to the clarification of disease etiology and might open new avenues for potential therapeutic interventions. This review aims at giving an overview of the roles of microgliamediated neuroinflammation in major retinal degenerative diseases like glaucoma, age-related macular degeneration, and diabetic retinopathy.

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“…It is a progressive disease affecting people above 40 years, optic nerve changes are the main features, intraocular pressure (IOP) is the famous measurable risk factor for POAG, but some cases with the reduction of their IOP either by medical or surgical treatment does not stop the progression of the disease. So, other factors as lack of neurological protection for ganglion cells in the retina and cell apoptosis mechanisms may also play roles in progression of glaucoma [1] [2] [3]. Another factor may be incriminated in the process of POAG such as oxidative stress, other inflammatory factors and characteristic pattern of cell death by apoptosis [4].…”

Section: Introductionmentioning

confidence: 99%

The Role of Serum Ceruloplasmin and Oxidative Stress Markers in Primary Open Angle Glaucoma

Sharkh¹,

Nada²,

Moety³

et al. 2018

OJOph

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Purpose: The study aimed at evaluation of the role of ceruloplasmin (A protein involved in iron homeostasis and can inactivate free radicals) and other oxidative stress markers as superoxide dismutase (SOD), malondialdehyde (MDA) and catalase activity (CAT) in primary open angle glaucoma (POAG). Methods: This observational case control study included 90 persons divided into 3 equal groups: group A of 30 normal persons as a control group, group B of 30 patients of untreated (POAG) (firstly diagnosed) by the clinical characters including measuring intraocular pressure (IOP), optic disc cupping and visual field changes and group C of 30 patients of POAG under medical treatment by topical anti-glaucomatous drugs. Serum ceruloplasmin, superoxide dismutase, malondialdehyde and catalase activity were measured in all groups, statistical analysis of the data was performed. Results: In a comparison to group A of control, serum ceruloplasmin decreased significantly in group B of untreated POAG (20.95 ± 6.01) mg-dl and in group C of POAG under treatment (22.15 ± 6.14) mg-dl (P < 0.001), and there was no statistically difference between group B and C (P > 0.05). Also, serum superoxide dismutase increased significantly in group B (2.23 ± 0.4) and in group C (2.19 ± 0.38) U-ml (P < 0.001), and there was no statistically difference between group B and C (P > 0.05). Serum malondialdehyde increased significantly in group B (3.82 ± 0.74) nmol-ml and in group C (3.55 ± 0.73) nmol-ml (P < 0.001) in a comparison to the control group A (2.23 ± 0.41) nmol-ml, and there was no statistically difference between group B and C (P > 0.05). Serum catalase decreased significantly in group B (17.97 ± 2.75) U-ml and in group C (18.75 ± 2.33) U-ml in a comparison to the control group A (22.67 ± 3.05) U-ml (P < 0.001), and there was no statistically difference between group B How to cite this paper:

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The Role of Inflammation in the Pathogenesis of Glaucoma

Cited by 188 publications

References 79 publications

Gap Junction Coupled Cells, Barriers and Systemic Inflammation

Gap Junction Coupled Cells, Barriers and Systemic Inflammation

Contribution of microglia‐mediated neuroinflammation to retinal degenerative diseases

The Role of Serum Ceruloplasmin and Oxidative Stress Markers in Primary Open Angle Glaucoma

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