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Novel Insights in Retinal Diseases Pathophysiology and Therapies

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 July 2022) | Viewed by 33610

Special Issue Editor

Prof. Dr. Settimio Rossi

E-Mail Website
Guest Editor
Multidisciplinary Department of Medical, Surgical and Dental Sciences, University of Campania L. Vanvitelli, Naples, Italy
Interests: inflammation; miRNA; eye; retina; gene therapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The research on retinal diseases has greatly developed and expanded, allowing us to obtain a better understanding of retinal diseases.

Chronic inflammation and neurodegeneration have a widely recognized role in the pathogenesis of the main retinal pathologies, such as age-related macular degeneration (AMD), diabetic retinopathy (DR), idiopathic vitreoretinal diseases, etc.

Common pathways have been identified among various retinal diseases that can be useful for the identification of new therapeutic targets and for the development of new treatment strategies.

Given the complexity of retinal pathologies, multidisciplinary approaches must be applied to provide solutions, as retinal problems appear to have mixed etiological origins.

The aim of this Research Topic is to clarify the pathogenesis of the main retinal diseases, in order to identify new ocular and systemic markers and new therapeutic strategies.

Prof. Dr. Settimio Rossi
Guest Editor

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • retinal diseases
  • age-related macular degeneration (AMD)
  • diabetic retinopathy (DR)
  • idiopathic vitreoretinal diseases
  • pathophysiology
  • therapeutic strategies
  • biomarkers

Published Papers (12 papers)

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Research

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25 pages, 15851 KiB  
Article
Molecular and Functional Characterization of BDNF-Overexpressing Human Retinal Pigment Epithelial Cells Established by Sleeping Beauty Transposon-Mediated Gene Transfer
by Larissa Mattern, Katrin Otten, Csaba Miskey, Matthias Fuest, Zsuzsanna Izsvák, Zoltán Ivics, Peter Walter, Gabriele Thumann and Sandra Johnen
Int. J. Mol. Sci. 2022, 23(21), 12982; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232112982 - 26 Oct 2022
Cited by 5 | Viewed by 1700
Abstract
More and more patients suffer from multifactorial neurodegenerative diseases, such as age-related macular degeneration (AMD). However, their pathological mechanisms are still poorly understood, which complicates the development of effective therapies. To improve treatment of multifactorial diseases, cell-based gene therapy can be used to [...] Read more.
More and more patients suffer from multifactorial neurodegenerative diseases, such as age-related macular degeneration (AMD). However, their pathological mechanisms are still poorly understood, which complicates the development of effective therapies. To improve treatment of multifactorial diseases, cell-based gene therapy can be used to increase the expression of therapeutic factors. To date, there is no approved therapy for dry AMD, including late-stage geographic atrophy. We present a treatment option for dry AMD that transfers the brain-derived neurotrophic factor (BDNF) gene into retinal pigment epithelial (RPE) cells by electroporation using the plasmid-based Sleeping Beauty (SB) transposon system. ARPE-19 cells and primary human RPE cells were co-transfected with two plasmids encoding the SB100X transposase and the transposon carrying a BDNF transcription cassette. We demonstrated efficient expression and secretion of BDNF in both RPE cell types, which were further increased in ARPE-19 cell cultures exposed to hydrogen peroxide. BDNF-transfected cells exhibited lower apoptosis rates and stimulated neurite outgrowth in human SH-SY5Y cells. This study is an important step in the development of a cell-based BDNF gene therapy that could be applied as an advanced therapy medicinal product to treat dry AMD or other degenerative retinal diseases. Full article
(This article belongs to the Special Issue Novel Insights in Retinal Diseases Pathophysiology and Therapies)
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15 pages, 2653 KiB  
Article
A Dpagt1 Missense Variant Causes Degenerative Retinopathy without Myasthenic Syndrome in Mice
by Lillian F. Hyde, Yang Kong, Lihong Zhao, Sriganesh Ramachandra Rao, Jieping Wang, Lisa Stone, Andrew Njaa, Gayle B. Collin, Mark P. Krebs, Bo Chang, Steven J. Fliesler, Patsy M. Nishina and Jürgen K. Naggert
Int. J. Mol. Sci. 2022, 23(19), 12005; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms231912005 - 09 Oct 2022
Cited by 2 | Viewed by 1786
Abstract
Congenital disorders of glycosylation (CDG) are a heterogenous group of primarily autosomal recessive mendelian diseases caused by disruptions in the synthesis of lipid-linked oligosaccharides and their transfer to proteins. CDGs usually affect multiple organ systems and vary in presentation, even within families. There [...] Read more.
Congenital disorders of glycosylation (CDG) are a heterogenous group of primarily autosomal recessive mendelian diseases caused by disruptions in the synthesis of lipid-linked oligosaccharides and their transfer to proteins. CDGs usually affect multiple organ systems and vary in presentation, even within families. There is currently no cure, and treatment is aimed at ameliorating symptoms and improving quality of life. Here, we describe a chemically induced mouse mutant, tvrm76, with early-onset photoreceptor degeneration. The recessive mutation was mapped to Chromosome 9 and associated with a missense mutation in the Dpagt1 gene encoding UDP-N-acetyl-D-glucosamine:dolichyl-phosphate N-acetyl-D-glucosaminephosphotransferase (EC 2.7.8.15). The mutation is predicted to cause a substitution of aspartic acid with glycine at residue 166 of DPAGT1. This represents the first viable animal model of a Dpagt1 mutation and a novel phenotype for a CDG. The increased expression of Ddit3, and elevated levels of HSPA5 (BiP) suggest the presence of early-onset endoplasmic reticulum (ER) stress. These changes were associated with the induction of photoreceptor apoptosis in tvrm76 retinas. Mutations in human DPAGT1 cause myasthenic syndrome-13 and severe forms of a congenital disorder of glycosylation Type Ij. In contrast, Dpagt1tvrm76 homozygous mice present with congenital photoreceptor degeneration without overt muscle or muscular junction involvement. Our results suggest the possibility of DPAGT1 mutations in human patients that present primarily with retinitis pigmentosa, with little or no muscle disease. Variants in DPAGT1 should be considered when evaluating cases of non-syndromic retinal degeneration. Full article
(This article belongs to the Special Issue Novel Insights in Retinal Diseases Pathophysiology and Therapies)
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15 pages, 2323 KiB  
Article
Systemic Beta-Hydroxybutyrate Affects BDNF and Autophagy into the Retina of Diabetic Mice
by Maria Consiglia Trotta, Carlo Gesualdo, Hildegard Herman, Sami Gharbia, Cornel Balta, Caterina Claudia Lepre, Marina Russo, Annalisa Itro, Giovanbattista D’Amico, Luisa Peluso, Iacopo Panarese, Gorizio Pieretti, Giuseppe Ferraro, Francesca Simonelli, Michele D’Amico, Settimio Rossi and Anca Hermenean
Int. J. Mol. Sci. 2022, 23(17), 10184; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms231710184 - 05 Sep 2022
Cited by 10 | Viewed by 2498
Abstract
Background: Diabetic retinopathy (DR) is a neurovascular disease, characterized by a deficiency of brain-derived neurotrophic factor (BDNF), a regulator of autophagy. Beta-hydroxybutyrate (BHB), previously reported as a protective agent in DR, has been associated with BDNF promotion. Here, we investigated whether systemic BHB [...] Read more.
Background: Diabetic retinopathy (DR) is a neurovascular disease, characterized by a deficiency of brain-derived neurotrophic factor (BDNF), a regulator of autophagy. Beta-hydroxybutyrate (BHB), previously reported as a protective agent in DR, has been associated with BDNF promotion. Here, we investigated whether systemic BHB affects the retinal levels of BDNF and local autophagy in diabetic mice with retinopathy; Methods: C57BL/6J mice were administered with intraperitoneal (i.p.) streptozotocin (STZ) (75 mg/kg) injection to develop diabetes. After 2 weeks, they received i.p. injections of BHB (25–50–100 mg/kg) twice a week for 10 weeks. Retinal samples were collected in order to perform immunofluorescence, Western blotting, and ELISA analysis; Results: BHB 50 mg/kg and 100 mg/kg significantly improved retinal BDNF levels (p < 0.01) in diabetic mice. This improvement was negatively associated with autophagosome–lysosome formations (marked by LC3B and ATG14) and to higher levels of connexin 43 (p < 0.01), a marker of cell integrity. Moreover, BHB administration significantly reduced M1 microglial activation and autophagy (p < 0.01); Conclusions: The systemic administration of BHB in mice with DR improves the retinal levels of BDNF, with the consequent reduction of the abnormal microglial autophagy. This leads to retinal cell safety through connexin 43 restoration. Full article
(This article belongs to the Special Issue Novel Insights in Retinal Diseases Pathophysiology and Therapies)
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16 pages, 4876 KiB  
Article
Role of Autotaxin in High Glucose-Induced Human ARPE-19 Cells
by Yang Liu, Reiko Yamagishi, Megumi Honjo, Makoto Kurano, Yutaka Yatomi, Koji Igarashi and Makoto Aihara
Int. J. Mol. Sci. 2022, 23(16), 9181; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23169181 - 16 Aug 2022
Cited by 1 | Viewed by 2054
Abstract
Autotaxin (ATX) is an enzymatic with lysophospholipase D (lysoPLD) activity. We investigated the role of ATX in high glucose (HG)-induced human retinal pigment epithelial (ARPE-19) cells to explore the pathogenesis of diabetic retinopathy (DR). We performed a quantitative real-time polymerase chain reaction, Western [...] Read more.
Autotaxin (ATX) is an enzymatic with lysophospholipase D (lysoPLD) activity. We investigated the role of ATX in high glucose (HG)-induced human retinal pigment epithelial (ARPE-19) cells to explore the pathogenesis of diabetic retinopathy (DR). We performed a quantitative real-time polymerase chain reaction, Western blotting, immunocytochemistry, enzyme-linked immunosorbent assay, cell permeability assay, and transepithelial electrical resistance measurement in HG-induced ARPE-19 cells and compared their results with those of normal glucose and osmotic pressure controls. ATX expression and its lysoPLD activity, barrier function, and expression of vascular endothelial growth factor receptors VEGFR-1 and VEGFR-2 were downregulated, while fibrotic responses, cytoskeletal reorganization, and transforming growth factor-β expression were upregulated, in the HG group. Our results suggest that HG induces intracellular ATX downregulation, barrier dysfunction, and fibrosis, which are involved in early DR and can be targeted for DR treatment. Full article
(This article belongs to the Special Issue Novel Insights in Retinal Diseases Pathophysiology and Therapies)
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20 pages, 3329 KiB  
Article
Phenotype Characterization of a Mice Genetic Model of Absolute Blindness
by Santiago Milla-Navarro, Mateo Pazo-González, Francisco Germain and Pedro de la Villa
Int. J. Mol. Sci. 2022, 23(15), 8152; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23158152 - 24 Jul 2022
Cited by 4 | Viewed by 1910
Abstract
Recent technological development requires new approaches to address the problem of blindness. Such approaches need to be able to ensure that no cells with photosensitive capability remain in the retina. The presented model, Opn4−/− × Pde6brd10/rd10 (O×Rd) double mutant murine, is [...] Read more.
Recent technological development requires new approaches to address the problem of blindness. Such approaches need to be able to ensure that no cells with photosensitive capability remain in the retina. The presented model, Opn4−/− × Pde6brd10/rd10 (O×Rd) double mutant murine, is a combination of a mutation in the Pde6b gene (photoreceptor degeneration) together with a deletion of the Opn4 gene (responsible for the expression of melanopsin in the intrinsically photosensitive retinal ganglion cells). This model has been characterized and compared with those of WT mice and murine animal models displaying both mutations separately. A total loss of pupillary reflex was observed. Likewise, behavioral tests demonstrated loss of rejection to illuminated spaces and a complete decrease in visual acuity (optomotor test). Functional recordings showed an absolute disappearance of various wave components of the full-field and pattern electroretinogram (fERG, pERG). Likewise, visual evoked potential (VEP) could not be recorded. Immunohistochemical staining showed marked degeneration of the outer retinal layers and the absence of melanopsin staining. The combination of both mutations has generated an animal model that does not show any photosensitive element in its retina. This model is a potential tool for the study of new ophthalmological approaches such as optosensitive agents. Full article
(This article belongs to the Special Issue Novel Insights in Retinal Diseases Pathophysiology and Therapies)
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16 pages, 3355 KiB  
Article
Enhanced cGMP Interactor Rap Guanine Exchange Factor 4 (EPAC2) Expression and Activity in Degenerating Photoreceptors: A Neuroprotective Response?
by Michel Rasmussen, Jiaming Zhou, Frank Schwede and Per Ekström
Int. J. Mol. Sci. 2022, 23(9), 4619; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23094619 - 21 Apr 2022
Cited by 3 | Viewed by 1557
Abstract
The disease retinitis pigmentosa (RP) leads to photoreceptor degeneration by a yet undefined mechanism(s). In several RP mouse models (i.e., rd mice), a high cyclic GMP (cGMP) level within photoreceptors is detected, suggesting that cGMP plays a role in degeneration. The rap guanine [...] Read more.
The disease retinitis pigmentosa (RP) leads to photoreceptor degeneration by a yet undefined mechanism(s). In several RP mouse models (i.e., rd mice), a high cyclic GMP (cGMP) level within photoreceptors is detected, suggesting that cGMP plays a role in degeneration. The rap guanine exchange factor 4 (EPAC2) is activated by cyclic AMP (cAMP) and is an accepted cGMP-interacting protein. It is unclear whether and how cGMP interacts with EPAC2 in degenerating photoreceptors; we therefore investigated EPAC2 expression and interactions with cGMP and cAMP in retinas of the rd1 and rd10 models for retinal degeneration. EPAC2 expression in the photoreceptor layer increased significantly during rd1 and rd10 degeneration, and an increase in EPAC2 interactions with cGMP but not cAMP in the rd1 was also seen via a proximity ligation assay on histological sections. Retinal explant cultures revealed that pharmacological inhibition of the EPAC2 activity reduced the photoreceptor layer thickness in the rd10 retina, suggesting that EPAC2 inhibition promotes degeneration. Taken together, our results support the hypothesis that high degeneration-related cGMP leads to increased EPAC2 and cGMP interactions, inhibiting EPAC2. By inference, EPAC2 could have neuroprotective capacities that may be exploited in the future. Full article
(This article belongs to the Special Issue Novel Insights in Retinal Diseases Pathophysiology and Therapies)
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14 pages, 4698 KiB  
Article
The Effect of Sodium-Dependent Glucose Cotransporter 2 Inhibitor Tofogliflozin on Neurovascular Coupling in the Retina in Type 2 Diabetic Mice
by Junya Hanaguri, Harumasa Yokota, Akifumi Kushiyama, Sakura Kushiyama, Masahisa Watanabe, Satoru Yamagami and Taiji Nagaoka
Int. J. Mol. Sci. 2022, 23(3), 1362; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23031362 - 25 Jan 2022
Cited by 17 | Viewed by 3088
Abstract
We investigated the effect of tofogliflozin, a sodium-dependent glucose cotransporter 2 inhibitor (SGLT2i), on retinal blood flow dysregulation, neural retinal dysfunction, and the impaired neurovascular coupling in type 2 diabetic mice. Tofogliflozin was added to mouse chow to deliver 5 mg/kg/day and 6-week-old [...] Read more.
We investigated the effect of tofogliflozin, a sodium-dependent glucose cotransporter 2 inhibitor (SGLT2i), on retinal blood flow dysregulation, neural retinal dysfunction, and the impaired neurovascular coupling in type 2 diabetic mice. Tofogliflozin was added to mouse chow to deliver 5 mg/kg/day and 6-week-old mice were fed for 8 weeks. The longitudinal changes in the retinal neuronal function and blood flow responses to systemic hyperoxia and flicker stimulation were evaluated every 2 weeks in diabetic db/db mice that received tofogliflozin (n =6) or placebo (n = 6) from 8 to 14 weeks of age. We also evaluated glial activation and vascular endothelial growth factor (VEGF) expression by immunofluorescence. Tofogliflozin treatment caused a sustained decrease in blood glucose in db/db mice from 8 weeks of the treatment. In tofogliflozin-treated db/db mice, both responses improved from 8 to 14 weeks of age, compared with vehicle-treated diabetic mice. Subsequently, the electroretinography implicit time for the oscillatory potential was significantly improved in SGLT2i-treated db/db mice. The systemic tofogliflozin treatment prevented the activation of glial fibrillary acidic protein and VEGF protein expression, as detected by immunofluorescence. Our results suggest that glycemic control with tofogliflozin significantly improved the impaired retinal neurovascular coupling in type 2 diabetic mice with the inhibition of retinal glial activation. Full article
(This article belongs to the Special Issue Novel Insights in Retinal Diseases Pathophysiology and Therapies)
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Review

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19 pages, 3507 KiB  
Review
Ocular Lymphatic and Glymphatic Systems: Implications for Retinal Health and Disease
by Nasir Uddin and Matt Rutar
Int. J. Mol. Sci. 2022, 23(17), 10139; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms231710139 - 04 Sep 2022
Cited by 5 | Viewed by 4670
Abstract
Clearance of ocular fluid and metabolic waste is a critical function of the eye in health and disease. The eye has distinct fluid outflow pathways in both the anterior and posterior segments. Although the anterior outflow pathway is well characterized, little is known [...] Read more.
Clearance of ocular fluid and metabolic waste is a critical function of the eye in health and disease. The eye has distinct fluid outflow pathways in both the anterior and posterior segments. Although the anterior outflow pathway is well characterized, little is known about posterior outflow routes. Recent studies suggest that lymphatic and glymphatic systems play an important role in the clearance of fluid and waste products from the posterior segment of the eye. The lymphatic system is a vascular network that runs parallel to the blood circulatory system. It plays an essential role in maintenance of fluid homeostasis and immune surveillance in the body. Recent studies have reported lymphatics in the cornea (under pathological conditions), ciliary body, choroid, and optic nerve meninges. The evidence of lymphatics in optic nerve meninges is, however, limited. An alternative lymphatic system termed the glymphatic system was recently discovered in the rodent eye and brain. This system is a glial cell-based perivascular network responsible for the clearance of interstitial fluid and metabolic waste. In this review, we will discuss our current knowledge of ocular lymphatic and glymphatic systems and their role in retinal degenerative diseases. Full article
(This article belongs to the Special Issue Novel Insights in Retinal Diseases Pathophysiology and Therapies)
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15 pages, 917 KiB  
Review
Resolution of Inflammation in Retinal Disorders: Briefly the State
by Maria Consiglia Trotta, Carlo Gesualdo, Francesco Petrillo, Caterina Claudia Lepre, Alberto Della Corte, Giancuomo Cavasso, Giulia Maggiore, Anca Hermenean, Francesca Simonelli, Michele D’Amico and Settimio Rossi
Int. J. Mol. Sci. 2022, 23(9), 4501; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23094501 - 19 Apr 2022
Cited by 9 | Viewed by 1949
Abstract
The most frequent retinal diseases, such as diabetic retinopathy, age-related macular degeneration and posterior uveitis, are underlined by oxidative stress or aging-induced retinal inflammation, which contributes to vision impairing or loss. Resolution of inflammation is emerging as a critical phase able to counteract [...] Read more.
The most frequent retinal diseases, such as diabetic retinopathy, age-related macular degeneration and posterior uveitis, are underlined by oxidative stress or aging-induced retinal inflammation, which contributes to vision impairing or loss. Resolution of inflammation is emerging as a critical phase able to counteract the inflammatory process leading to the progression of retinal damage. Particularly, pro-resolving mediators (PMs) play a key role in the modulation of inflammatory exudates and could be considered a new target to be investigated in different inflammatory-autoimmune pathologies. Here, we highlight the most recent studies concerning the role of the main PMs (lipoxins, resolvins, prtectins, maresins and annexins) in retinal inflammation, in order to collect the best evidence in the field of inflammatory retinal damage resolution and to propose novel pharmacological approaches in the management of the most common retinal diseases. Full article
(This article belongs to the Special Issue Novel Insights in Retinal Diseases Pathophysiology and Therapies)
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22 pages, 1129 KiB  
Review
Diabetic Retinopathy: From Animal Models to Cellular Signaling
by Priyamvada M. Pitale and Marina S. Gorbatyuk
Int. J. Mol. Sci. 2022, 23(3), 1487; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23031487 - 27 Jan 2022
Cited by 28 | Viewed by 5663
Abstract
Diabetic retinopathy (DR) is an ocular complication of diabetes mellitus (DM), a metabolic disorder characterized by elevation in blood glucose level. The pathogenesis of DR includes vascular, neuronal, and inflammatory components leading to activation of complex cellular molecular signaling. If untreated, the disease [...] Read more.
Diabetic retinopathy (DR) is an ocular complication of diabetes mellitus (DM), a metabolic disorder characterized by elevation in blood glucose level. The pathogenesis of DR includes vascular, neuronal, and inflammatory components leading to activation of complex cellular molecular signaling. If untreated, the disease can culminate in vision loss that eventually leads to blindness. Animal models mimicking different aspects of DM complications have been developed to study the development and progression of DR. Despite the significant contribution of the developed DR models to discovering the mechanisms of DR and the recent achievements in the research field, the sequence of cellular events in diabetic retinas is still under investigation. Partially, this is due to the complexity of molecular mechanisms, although the lack of availability of models that adequately mimic all the neurovascular pathobiological features observed in patients has also contributed to the delay in determining a precise molecular trigger. In this review, we provide an update on the status of animal models of DR to help investigators choose an appropriate system to validate their hypothesis. We also discuss the key cellular and physiological events of DR in these models. Full article
(This article belongs to the Special Issue Novel Insights in Retinal Diseases Pathophysiology and Therapies)
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14 pages, 301 KiB  
Review
Where Are We with RPE Replacement Therapy? A Translational Review from the Ophthalmologist Perspective
by Raffaele Raimondi, Piero Zollet, Francesco Paolo De Rosa, Panagiotis Tsoutsanis, Matteo Stravalaci, Marianna Paulis, Antonio Inforzato and Mario R. Romano
Int. J. Mol. Sci. 2022, 23(2), 682; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23020682 - 08 Jan 2022
Cited by 9 | Viewed by 3030
Abstract
The retinal pigmented epithelium (RPE) plays a pivotal role in retinal homeostasis. It is therefore an interesting target to fill the unmet medical need of different retinal diseases, including age-related macular degeneration and Stargardt disease. RPE replacement therapy may use different cellular sources: [...] Read more.
The retinal pigmented epithelium (RPE) plays a pivotal role in retinal homeostasis. It is therefore an interesting target to fill the unmet medical need of different retinal diseases, including age-related macular degeneration and Stargardt disease. RPE replacement therapy may use different cellular sources: induced pluripotent stem cells or embryonic stem cells. Cells can be transferred as suspension on a patch with different surgical approaches. Results are promising although based on very limited samples. In this review, we summarize the current progress of RPE replacement and provide a comparative assessment of different published approaches which may become standard of care in the future. Full article
(This article belongs to the Special Issue Novel Insights in Retinal Diseases Pathophysiology and Therapies)
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11 pages, 1469 KiB  
Review
Vitreoretinal Surgery in the Prevention and Treatment of Toxic Tumour Syndrome in Uveal Melanoma: A Systematic Review
by Mario R. Romano, Fiammetta Catania, Filippo Confalonieri, Piero Zollet, Davide Allegrini, Jessica Sergenti, Francesco B. Lanza, Mariantonia Ferrara and Martina Angi
Int. J. Mol. Sci. 2021, 22(18), 10066; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms221810066 - 17 Sep 2021
Cited by 6 | Viewed by 2027
Abstract
Toxic tumour syndrome (TTS) is a particularly aggressive form of secondary vasculopathy occurring after radiation therapy of uveal melanoma due to the persistence of the necrotic tumour mass inside the eye. The development of TTS confers a particularly unfavourable functional and anatomical ocular [...] Read more.
Toxic tumour syndrome (TTS) is a particularly aggressive form of secondary vasculopathy occurring after radiation therapy of uveal melanoma due to the persistence of the necrotic tumour mass inside the eye. The development of TTS confers a particularly unfavourable functional and anatomical ocular prognosis, ultimately requiring enucleation in most cases if untreated. Vitreoretinal (VR) surgery has been successfully applied for treatment and prevention of TTS using both resecting and non-resecting techniques. In this systematic review, we aim to define characteristics of uveal melanomas benefiting the most from secondary VR surgery and to outline the optimal type and timing of VR intervention in such cases. Analysis of the literature reveals that endoresection should be performed within 3 months after radiotherapy to tumours thicker than 7 mm and with a largest basal diameter between 8 mm and 15 mm with post-equatorial location, especially after proton beam treatment. Alternatively, endodrainage remains a valid therapeutic option in eyes with macula-off retinal detachment, tumour diameter larger than 15 mm or ciliary body involvement. VR surgery can be successful in the management of TTS following radiotherapy for uveal melanoma when timing and indication are appropriately evaluated. Full article
(This article belongs to the Special Issue Novel Insights in Retinal Diseases Pathophysiology and Therapies)
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