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Glaucoma – Pathophysiology and Therapeutic Options

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A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Neuroscience".

Deadline for manuscript submissions: closed (31 October 2021) | Viewed by 39765

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Special Issue Editors

Dr. Jacqueline Reinhard

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Guest Editor

Department of Cell Morphology and Molecular Neurobiology, Ruhr-University Bochum, Bochum, Germany
Interests: glaucoma; intraocular pressure; ischemia; retinal diseases; therapy approaches

Prof. Dr. Stephanie C. Joachim

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Guest Editor

Experimental Eye Research Institute, University Eye Hospital, Ruhr-University Bochum, 44892 Bochum, Germany
Interests: glaucoma; age-related macular degeneration; retinal diseases; retinal organ culture models; autoimmunity; neuroprotection
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Special Issue Information

Dear Colleagues,

Glaucoma is one of the leading causes of irreversible blindness worldwide, and the prevalence is rising continuously. Indeed, the number of people affected will likely increase from around 76 million in 2020 to approximately 112 million in 2040. Glaucoma comprises a group of chronic, progressive optic neuropathies. These are characterized by changes in the optic nerve head, retinal ganglion cell degeneration, and thinning of the nerve fiber layer, leading to visual field loss. Intraocular pressure (IOP) elevation is still the main risk factor for glaucoma progression, which leads to mechanical tension, a remodeling of the lamina cribrosa, ischemic damage, axonal disorders, as well as neurodegeneration. Therefore, a cornerstone of glaucoma treatment is lowering of the IOP. Importantly, glaucoma is a multifactorial neurodegenerative disease and glaucomatous optic neuropathies can also occur in people with a normal physiological IOP, defined as normal tension glaucoma. Here, other causes are assumed, e.g., immunological reactions, circulatory disturbances, hypoxia, and oxidative stress. However, the exact pathophysiology, particularly the underlying molecular signaling mechanisms of IOP-induced and IOP-independent glaucomatous neurodegeneration, is not yet understood sufficiently.

Invited research articles, review articles, and short communications of this Special Issue will specifically focus on the current state of knowledge regarding IOP-dependent as well as IOP-independent glaucomatous neuropathies. Experts in the field will be invited to submit articles that, inter alia, shed light on basic and clinical research, experimental in vivo and in vitro models, novel IOP-lowering surgeries and therapies, IOP-independent neuroprotective strategies, biomarker identification, as well as molecular signaling mechanisms.

Dr. Jacqueline Reinhard
Prof. Dr. Stephanie C. Joachim
Guest Editors

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Keywords

Glaucoma
Immunological reactions
Intraocular pressure elevation
In vivo and in vitro models
Ischemia
Molecular signaling pathways
Ocular hypertension
Optic nerve/optic head damage
Retinal neurodegeneration
Therapy

Published Papers (12 papers)

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Research

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21 pages, 43005 KiB

Open AccessArticle

Proteomic Analysis of Retinal Tissue in an S100B Autoimmune Glaucoma Model

by Sabrina Reinehr, Annika Guntermann, Janine Theile, Lara Benning, Pia Grotegut, Sandra Kuehn, Bettina Serschnitzki, H. Burkhard Dick, Katrin Marcus, Stephanie C. Joachim and Caroline May

Biology 2022, 11(1), 16; https://0-doi-org.brum.beds.ac.uk/10.3390/biology11010016 - 23 Dec 2021

Cited by 3 | Viewed by 3070

Abstract

Glaucoma is a neurodegenerative disease that leads to damage of retinal ganglion cells and the optic nerve. Patients display altered antibody profiles and increased antibody titer, e.g., against S100B. To identify the meaning of these antibodies, animals were immunized with S100B. Retinal ganglion cell loss, optic nerve degeneration, and increased glial cell activity were noted. Here, we aimed to gain more insights into the pathophysiology from a proteomic point of view. Hence, rats were immunized with S100B, while controls received sodium chloride. After 7 and 14 days, retinae were analyzed through mass spectrometry and immunohistology. Using data-independent acquisition-based mass spectrometry, we identified more than 1700 proteins on a high confidence level for both study groups, respectively. Of these 1700, 43 proteins were significantly altered in retinae after 7 days and 67 proteins revealed significant alterations at 14 days. For example, α2-macroglobulin was found significantly increased not only by mass spectrometry analysis, but also with immunohistological staining in S100B retinae at 7 and 14 days. All in all, the identified proteins are often associated with the immune system, such as heat shock protein 60. Once more, these data underline the important role of immunological factors in glaucoma pathogenesis. Full article

(This article belongs to the Special Issue Glaucoma – Pathophysiology and Therapeutic Options)

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11 pages, 2166 KiB

Open AccessArticle

Intraocular Pressure Changes during Hemodiafiltration with Two different Concentrations of Sodium in the Dialysate

by Claudia Lerma, Nadia Saavedra-Fuentes, Jasbeth Ledesma-Gil, Martín Calderón-Juárez, Héctor Pérez-Grovas and Salvador López-Gil

Biology 2022, 11(1), 12; https://0-doi-org.brum.beds.ac.uk/10.3390/biology11010012 - 23 Dec 2021

Cited by 2 | Viewed by 2580

Abstract

Ocular complications are common among end-stage renal disease patients and some complications had been linked to increments of intraocular pressure (IOP) during hemodialysis. The changes of IOP during hemodiafiltration (HDF) have been scarcely investigated and the potential influence of the sodium dialysate concentration is unknown. The aim of this study was to compare the IOP changes during HDF with sodium dialysate concentration, either fixed or individualized. Thirteen end-stage renal disease patients participated in the study; they were treated with HDF using a dialysate sodium profile fixed at 138 mmol and another session with an individualized sodium profile. The intraocular pressure was measured before and after each session and every 30 min during HDF. Both groups had a similar HDF prescription, blood pressure, and biochemical parameters. At the end of hemodiafiltration, sodium concentration decreased only in the fixed sodium profile group. The number of patients with at least an episode of intraocular hypertension during HDF ranged from 5 (19%) to 8 (31%) without significant differences between right and left eye nor between dialysate sodium concentration. During HDF, there is a large variability of IOP; transient events of intraocular hypertension are highly prevalent in this sample, and they are not related to the sodium dialysate concentration. Full article

(This article belongs to the Special Issue Glaucoma – Pathophysiology and Therapeutic Options)

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17 pages, 2320 KiB

Open AccessArticle

Targeted Lipidomic Analysis of Aqueous Humor Reveals Signaling Lipid-Mediated Pathways in Primary Open-Angle Glaucoma

by Nadezhda V. Azbukina, Dmitry V. Chistyakov, Sergei V. Goriainov, Vladislav I. Kotelin, Elena V. Fedoseeva, Sergey Yu. Petrov, Marina G. Sergeeva, Elena N. Iomdina and Evgeni Yu. Zernii

Biology 2021, 10(7), 658; https://0-doi-org.brum.beds.ac.uk/10.3390/biology10070658 - 13 Jul 2021

Cited by 14 | Viewed by 3356

Abstract

Primary open-angle glaucoma (POAG) is characterized by degeneration of retinal ganglion cells associated with an increase in intraocular pressure (IOP) due to hindered aqueous humor (AH) drainage through the trabecular meshwork and uveoscleral pathway. Polyunsaturated fatty acids and oxylipins are signaling lipids regulating neuroinflammation, neuronal survival and AH outflow. Among them, prostaglandins have been previously implicated in glaucoma and employed for its treatment. This study addressed the role of signaling lipids in glaucoma by determining their changes in AH accompanying IOP growth and progression of the disease. Eye liquids were collected from patients with POAG of different stages and cataract patients without glaucoma. Lipids were identified and quantified by UPLC-MS/MS. The compounds discriminating glaucoma groups were recognized using ANCOVA and PLS-DA statistic approaches and their biosynthetic pathways were predicted by bioinformatics. Among 22 signaling lipids identified in AH, stage/IOP-dependent alterations in glaucoma were provided by a small set of mediators, including 12,13-DiHOME, 9- and 13-HODE/KODE, arachidonic acid and lyso-PAF. These observations correlated with the expression of cytochromes P450 (CYPs) and phospholipases A2 in the ocular tissues. Interestingly, tear fluid exhibited similar lipidomic alterations in POAG. Overall, POAG may involve arachidonic acid/PAF-dependent pathways and oxidative stress as evidenced from an increase in its markers, KODEs and 12,13-DiHOME. The latter is a product of CYPs, one of which, CYP1B1, is known as POAG and primary congenital glaucoma-associated gene. These data provide novel targets for glaucoma treatment. Oxylipin content of tear fluid may have diagnostic value in POAG. Full article

(This article belongs to the Special Issue Glaucoma – Pathophysiology and Therapeutic Options)

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11 pages, 1343 KiB

Open AccessArticle

Erlanger Glaucoma Registry: Effect of a Long-Term Therapy with Statins and Acetyl Salicylic Acid on Glaucoma Conversion and Progression

by Nina Thiermeier, Robert Lämmer, Christian Mardin and Bettina Hohberger

Biology 2021, 10(6), 538; https://0-doi-org.brum.beds.ac.uk/10.3390/biology10060538 - 16 Jun 2021

Cited by 5 | Viewed by 2721

Abstract

Purpose: Drugs with cardiovascular protective properties (statins, acetylsalicylic acid (ASS)) were assumed to have positive effects on patients suffering from glaucoma disease. The present retrospective study aimed to investigate the influence of statins, ASS or a combination of both on the glaucoma conversion and progression rate in glaucoma suspects and glaucoma patients with a 20-year follow-up period. Methods: A retrospective analysis of 199 eyes of 120 patients (63 male, 57 female) of the Erlanger Glaucoma Registry (EGR; ClinicalTrials.gov Identifier: NCT00494923; ISSN 2191-5008, CS-2011) was performed considering systemic therapy with statins, ASS or a combination of both: 107 eyes with ocular hypertension (OHT) and 92 eyes with pre-perimetric primary open-angle glaucoma (pre-POAG). All patients received an ophthalmological examination including morphometric and functional glaucoma diagnostics. Glaucoma conversion was defined as the conversion of OHT to pre-POAG. Glaucoma progression was defined as confirmed visual field loss. Data were shown as percentages. Statistical analysis was performed by Chi-Quadrat tests. Results: 1. Glaucoma conversion/progression was observed in 46.7% of the subjects, additionally in combination with hypercholesterinemia in 76.8%. 2. Statins: 27.3% of eyes under systemic statin therapy showed a conversion/progression. Patients taking statins ≥ 10 years yielded a reduced conversion/progression rate (p = 0.028, non-significant after Bonferroni–Holm). 3. ASS: 34.7% of eyes under systemic ASS therapy showed a conversion/progression. A significantly lower conversion/progression rate was observed after ASS therapy ≥ 12 years (p = 0.017, significant after Bonferroni–Holm). 4. ASS and statins: 25.0% of eyes under combined therapy showed a conversion/progression. A significantly reduced conversion/progression rate was reached after 8 years of combined therapy (p = 0.049, non-significant after Bonferroni–Holm). Conclusions: Patients with ocular hypertension and early glaucoma seem to benefit from adjuvant cardiovascular protective therapy. However, the benefits and disadvantages of treatment with statins and/or ASS should be kept in mind. Thus, a thorough risk–benefit evaluation has to be performed for each patient individually to avoid unwanted side effects. Full article

(This article belongs to the Special Issue Glaucoma – Pathophysiology and Therapeutic Options)

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20 pages, 32286 KiB

Open AccessArticle

Reduced Retinal Degeneration in an Oxidative Stress Organ Culture Model through an iNOS-Inhibitor

by Ana M. Mueller-Buehl, Teresa Tsai, José Hurst, Carsten Theiss, Laura Peters, Lisa Hofmann, Fenja Herms, Sandra Kuehn, Sven Schnichels and Stephanie C. Joachim

Biology 2021, 10(5), 383; https://0-doi-org.brum.beds.ac.uk/10.3390/biology10050383 - 28 Apr 2021

Cited by 9 | Viewed by 2105

Abstract

In retinal organ cultures, H₂O₂ can be used to simulate oxidative stress, which plays a role in the development of several retinal diseases including glaucoma. We investigated whether processes underlying oxidative stress can be prevented in retinal organ cultures by an inducible nitric oxide synthase (iNOS)-inhibitor. To this end, porcine retinal explants were cultivated for four and eight days. Oxidative stress was induced via 300 µM H₂O₂ on day one for three hours. Treatment with the iNOS-inhibitor 1400 W was applied simultaneously, remaining for 72 h. Retinal ganglion cells (RGC), bipolar and amacrine cells, apoptosis, autophagy, and hypoxia were evaluated immunohistologically and by RT-qPCR. Additionally, RGC morphology was analyzed via transmission electron microscopy. H₂O₂-induced RGCs loss after four days was prevented by the iNOS-inhibitor. Additionally, electron microscopy revealed a preservation from oxidative stress in iNOS-inhibitor treated retinas at four and eight days. A late rescue of bipolar cells was seen in iNOS-inhibitor treated retinas after eight days. Hypoxic stress and apoptosis almost reached the control situation after iNOS-inhibitor treatment, especially after four days. In sum, the iNOS-inhibitor was able to prevent strong H₂O-induced degeneration in porcine retinas. Hence, this inhibitor seems to be a promising treatment option for retinal diseases. Full article

(This article belongs to the Special Issue Glaucoma – Pathophysiology and Therapeutic Options)

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15 pages, 983 KiB

Open AccessArticle

Functional Monitoring after Trabeculectomy or XEN Microstent Implantation Using Spectral Domain Optical Coherence Tomography and Visual Field Indices—A Retrospective Comparative Cohort Study

by Marc Schargus, Catharina Busch, Matus Rehak, Jie Meng, Manuela Schmidt, Caroline Bormann and Jan Darius Unterlauft

Biology 2021, 10(4), 273; https://0-doi-org.brum.beds.ac.uk/10.3390/biology10040273 - 27 Mar 2021

Cited by 8 | Viewed by 1876

Abstract

The aim of this study was to compare the efficacy of trabeculectomy (TE), single XEN microstent implantation (solo XEN) or combined XEN implantation and cataract surgery (combined XEN) in primary open-angle glaucoma cases, naïve to prior surgical treatment, using a monocentric retrospective comparative cohort study. Intraocular pressure (IOP) and the number of IOP-lowering drugs (Meds) were monitored during the first 24 months after surgery. Further disease progression was monitored using peripapillary retinal nerve fiber layer (RNFL) thickness examinations using spectral domain optical coherence tomography (OCT) as well as visual acuity (VA) and visual field (VF) tests. In the TE group (52 eyes), the mean IOP decreased from 24.9 ± 5.9 to 13.9 ± 4.2 mmHg (p < 0.001) and Meds decreased from 3.2 ± 1.2 to 0.5 ± 1.1 (p < 0.001). In the solo XEN (38 eyes) and the combined XEN groups, the mean IOP decreased from 24.1 ± 4.7 to 15.7 ± 3.0 mmHg (p < 0.001) and 25.4 ± 5.6 to 14.7 ± 3.2 mmHg (p < 0.001), while Meds decreased from 3.3 ± 0.8 to 0.8 ± 1.2 (p < 0.001) and 2.7 ± 1.2 to 0.4 ± 1.0 (p < 0.001), respectively. The VF and VA indices showed no sign of further deterioration, the RNFL thickness further decreased in all treatment groups after surgery. TE and XEN led to comparable reductions in IOP and Meds. Although the VA and VF indices remained unaltered, the RNFL thickness continuously decreased in all treatment groups during the 24-month follow-up. Full article

(This article belongs to the Special Issue Glaucoma – Pathophysiology and Therapeutic Options)

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15 pages, 5356 KiB

Open AccessArticle

The Paediatric Glaucoma Diagnostic Ability of Optical Coherence Tomography: A Comparison of Macular Segmentation and Peripapillary Retinal Nerve Fibre Layer Thickness

by Mael Lever, Christian Halfwassen, Jan Darius Unterlauft, Nikolaos E. Bechrakis, Anke Manthey and Michael R. R. Böhm

Biology 2021, 10(4), 260; https://0-doi-org.brum.beds.ac.uk/10.3390/biology10040260 - 25 Mar 2021

Cited by 8 | Viewed by 2218

Abstract

Paediatric glaucoma leads to a decreased thickness of the peripapillary retinal nerve fibre layer (pRNFL) and of the macula. These changes can be precisely quantified using spectral domain-optical coherence tomography (SD-OCT). Despite abundant reports in adults, studies on the diagnostic capacity of macular SD-OCT in paediatric glaucoma are rare. The aim of this study was to compare the glaucoma discriminative ability of pRNFL and macular segment thickness in paediatric glaucoma patients and healthy children. Data of 72 children aged 5–17 years (glaucoma: 19 (26.4%), healthy: 53 (73.6%)) examined with SD-OCT (SPECTRALIS^®, Heidelberg Engineering) were analysed retrospectively. The thickness of pRNFL sectors and of macular segment subfields were compared between diseased and healthy participants. Areas under the receiver-operating characteristic curves (AUC), sensitivity, and specificity from logistic regression were used to evaluate the glaucoma discriminative capacity of single and combined pRNFL and macular segments’ thickness. The results revealed a reduced thickness of the pRNFL and of the three inner macular layers in glaucoma patients, which correlates highly with the presence of glaucoma. The highest glaucoma discriminative ability was observed for the combination of pRNFL sectors or inner macular segments (AUC: 0.83 and 0.85, respectively), although sensitivity remained moderate (both 63% at 95% specificity). In conclusion, while confirmation from investigations in larger cohorts is required, SD-OCT-derived pRNFL and macular thickness measurements seem highly valuable for the diagnosis of paediatric glaucoma. Full article

(This article belongs to the Special Issue Glaucoma – Pathophysiology and Therapeutic Options)

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21 pages, 5165 KiB

Open AccessArticle

Extracellular Matrix Remodeling in the Retina and Optic Nerve of a Novel Glaucoma Mouse Model

by Jacqueline Reinhard, Susanne Wiemann, Sebastian Hildebrandt and Andreas Faissner

Biology 2021, 10(3), 169; https://0-doi-org.brum.beds.ac.uk/10.3390/biology10030169 - 24 Feb 2021

Cited by 13 | Viewed by 3538

Abstract

Glaucoma is a neurodegenerative disease that is characterized by the loss of retinal ganglion cells (RGC) and optic nerve fibers. Increased age and intraocular pressure (IOP) elevation are the main risk factors for developing glaucoma. Mice that are heterozygous (HET) for the mega-karyocyte protein tyrosine phosphatase 2 (PTP-Meg2) show chronic and progressive IOP elevation, severe RGCs loss, and optic nerve damage, and represent a valuable model for IOP-dependent primary open-angle glaucoma (POAG). Previously, evidence accumulated suggesting that glaucomatous neurodegeneration is associated with the extensive remodeling of extracellular matrix (ECM) molecules. Unfortunately, little is known about the exact ECM changes in the glaucomatous retina and optic nerve. Hence, the goal of the present study was to comparatively explore ECM alterations in glaucomatous PTP-Meg2 HET and control wild type (WT) mice. Due to their potential relevance in glaucomatous neurodegeneration, we specifically analyzed the expression pattern of the ECM glycoproteins fibronectin, laminin, tenascin-C, and tenascin-R as well as the proteoglycans aggrecan, brevican, and members of the receptor protein tyrosine phosphatase beta/zeta (RPTPβ/ζ) family. The analyses were carried out in the retina and optic nerve of glaucomatous PTP-Meg2 HET and WT mice using quantitative real-time PCR (RT-qPCR), immunohistochemistry, and Western blot. Interestingly, we observed increased fibronectin and laminin levels in the glaucomatous HET retina and optic nerve compared to the WT group. RT-qPCR analyses of the laminins α4, β2 and γ3 showed an altered isoform-specific regulation in the HET retina and optic nerve. In addition, an upregulation of tenascin-C and its interaction partner RPTPβ/ζ/phosphacan was found in glaucomatous tissue. However, comparable protein and mRNA levels for tenascin-R as well as aggrecan and brevican were observed in both groups. Overall, our study showed a remodeling of various ECM components in the glaucomatous retina and optic nerve of PTP-Meg2 HET mice. This dysregulation could be responsible for pathological processes such as neovascularization, inflammation, and reactive gliosis in glaucomatous neurodegeneration. Full article

(This article belongs to the Special Issue Glaucoma – Pathophysiology and Therapeutic Options)

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Review

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27 pages, 4085 KiB

Open AccessReview

Advanced Diffusion MRI of the Visual System in Glaucoma: From Experimental Animal Models to Humans

by Monica Mendoza, Max Shotbolt, Muneeb A. Faiq, Carlos Parra and Kevin C. Chan

Biology 2022, 11(3), 454; https://0-doi-org.brum.beds.ac.uk/10.3390/biology11030454 - 16 Mar 2022

Cited by 5 | Viewed by 5768

Abstract

Glaucoma is a group of ophthalmologic conditions characterized by progressive retinal ganglion cell death, optic nerve degeneration, and irreversible vision loss. While intraocular pressure is the only clinically modifiable risk factor, glaucoma may continue to progress at controlled intraocular pressure, indicating other major factors in contributing to the disease mechanisms. Recent studies demonstrated the feasibility of advanced diffusion magnetic resonance imaging (dMRI) in visualizing the microstructural integrity of the visual system, opening new possibilities for non-invasive characterization of glaucomatous brain changes for guiding earlier and targeted intervention besides intraocular pressure lowering. In this review, we discuss dMRI methods currently used in visual system investigations, focusing on the eye, optic nerve, optic tract, subcortical visual brain nuclei, optic radiations, and visual cortex. We evaluate how conventional diffusion tensor imaging, higher-order diffusion kurtosis imaging, and other extended dMRI techniques can assess the neuronal and glial integrity of the visual system in both humans and experimental animal models of glaucoma, among other optic neuropathies or neurodegenerative diseases. We also compare the pros and cons of these methods against other imaging modalities. A growing body of dMRI research indicates that this modality holds promise in characterizing early glaucomatous changes in the visual system, determining the disease severity, and identifying potential neurotherapeutic targets, offering more options to slow glaucoma progression and to reduce the prevalence of this world’s leading cause of irreversible but preventable blindness. Full article

(This article belongs to the Special Issue Glaucoma – Pathophysiology and Therapeutic Options)

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32 pages, 1662 KiB

Open AccessReview

Antibody and Protein Profiles in Glaucoma: Screening of Biomarkers and Identification of Signaling Pathways

by Nadine Auler, Henrik Tonner, Norbert Pfeiffer and Franz H. Grus

Biology 2021, 10(12), 1296; https://0-doi-org.brum.beds.ac.uk/10.3390/biology10121296 - 08 Dec 2021

Cited by 5 | Viewed by 2918

Abstract

Glaucoma represents a group of chronic neurodegenerative diseases, constituting the second leading cause of blindness worldwide. To date, chronically elevated intraocular pressure has been identified as the main risk factor and the only treatable symptom. However, there is increasing evidence in the recent literature that IOP-independent molecular mechanisms also play an important role in the progression of the disease. In recent years, it has become increasingly clear that glaucoma has an autoimmune component. The main focus nowadays is elucidating glaucoma pathogenesis, finding early diagnostic options and new therapeutic approaches. This review article summarizes the impact of different antibodies and proteins associated with glaucoma that can be detected for example by microarray and mass spectrometric analyzes, which (i) provide information about expression profiles and associated molecular signaling pathways, (ii) can possibly be used as a diagnostic tool in future and, (iii) can identify possible targets for therapeutic approaches. Full article

(This article belongs to the Special Issue Glaucoma – Pathophysiology and Therapeutic Options)

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25 pages, 1364 KiB

Open AccessEditor’s ChoiceReview

Cell-Based Neuroprotection of Retinal Ganglion Cells in Animal Models of Optic Neuropathies

by Yue Hu, Lynn Michelle Grodzki, Susanne Bartsch and Udo Bartsch

Biology 2021, 10(11), 1181; https://0-doi-org.brum.beds.ac.uk/10.3390/biology10111181 - 15 Nov 2021

Cited by 4 | Viewed by 2888

Abstract

Retinal ganglion cells (RGCs) comprise a heterogenous group of projection neurons that transmit visual information from the retina to the brain. Progressive degeneration of these cells, as it occurs in inflammatory, ischemic, traumatic or glaucomatous optic neuropathies, results in visual deterioration and is among the leading causes of irreversible blindness. Treatment options for these diseases are limited. Neuroprotective approaches aim to slow down and eventually halt the loss of ganglion cells in these disorders. In this review, we have summarized preclinical studies that have evaluated the efficacy of cell-based neuroprotective treatment strategies to rescue retinal ganglion cells from cell death. Intraocular transplantations of diverse genetically nonmodified cell types or cells engineered to overexpress neurotrophic factors have been demonstrated to result in significant attenuation of ganglion cell loss in animal models of different optic neuropathies. Cell-based combinatorial neuroprotective approaches represent a potential strategy to further increase the survival rates of retinal ganglion cells. However, data about the long-term impact of the different cell-based treatment strategies on retinal ganglion cell survival and detailed analyses of potential adverse effects of a sustained intraocular delivery of neurotrophic factors on retina structure and function are limited, making it difficult to assess their therapeutic potential. Full article

(This article belongs to the Special Issue Glaucoma – Pathophysiology and Therapeutic Options)

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40 pages, 1809 KiB

Open AccessReview

Candidate Glaucoma Biomarkers: From Proteins to Metabolites, and the Pitfalls to Clinical Applications

by Andrés Fernández-Vega Cueto, Lydia Álvarez, Montserrat García, Ana Álvarez-Barrios, Enol Artime, Luis Fernández-Vega Cueto, Miguel Coca-Prados and Héctor González-Iglesias

Biology 2021, 10(8), 763; https://0-doi-org.brum.beds.ac.uk/10.3390/biology10080763 - 10 Aug 2021

Cited by 17 | Viewed by 4588

Abstract

Glaucoma is an insidious group of eye diseases causing degeneration of the optic nerve, progressive loss of vision, and irreversible blindness. The number of people affected by glaucoma is estimated at 80 million in 2021, with 3.5% prevalence in people aged 40–80. The main biomarker and risk factor for the onset and progression of glaucoma is the elevation of intraocular pressure. However, when glaucoma is diagnosed, the level of retinal ganglion cell death usually amounts to 30–40%; hence, the urgent need for its early diagnosis. Molecular biomarkers of glaucoma, from proteins to metabolites, may be helpful as indicators of pathogenic processes observed during the disease’s onset. The discovery of human glaucoma biomarkers is hampered by major limitations, including whether medications are influencing the expression of molecules in bodily fluids, or whether tests to validate glaucoma biomarker candidates should include human subjects with different types and stages of the disease, as well as patients with other ocular and neurodegenerative diseases. Moreover, the proper selection of the biofluid or tissue, as well as the analytical platform, should be mandatory. In this review, we have summarized current knowledge concerning proteomics- and metabolomics-based glaucoma biomarkers, with specificity to human eye tissue and fluid, as well the analytical approach and the main results obtained. The complex data published to date, which include at least 458 different molecules altered in human glaucoma, merit a new, integrative approach allowing for future diagnostic tests based on the absolute quantification of local and/or systemic biomarkers of glaucoma. Full article

(This article belongs to the Special Issue Glaucoma – Pathophysiology and Therapeutic Options)

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