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Optic Neuropathies: From Molecular Mechanism to Therapy

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (30 May 2023) | Viewed by 8465

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Special Issue Editor

Dr. Yueh Chien

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Guest Editor

Department of Medical Research, Taipei Veteran General Hospital, Taipei 11217, Taiwan
Interests: stem cell; regeneration medicine; ophthalmology; nanomedicine

Special Issue Information

Dear Colleagues,

Optic neuropathy is damage inflicted on the optic nerve, which contains a bundle of axons from retinal ganglion cells (RGCs). Although optic neuropathy is a frequent cause of vision loss among people over 50 years old, it can occur in anyone regardless of age with diverse etiologies. Demyelinating, inflammatory, ischemic, and traumatic causes may result in the rapid onset of optic neuropathy, while toxic, metabolic, and genetic causes may contribute to the gradual course of chronic optic neuropathy. So far there is no effective therapy that can cure optic neuropathies, and the predominant consideration of treatment focuses on reducing symptoms and preventing further damage. Advances in our understanding of the molecular mechanisms supporting RGC loss in these disorders pave the way for novel therapeutic methods. This Special Issue aims to present the latest research on the preventive, regenerative, and therapeutic molecular strategies for optic neuropathies. We are pleased to announce that we are now soliciting manuscripts for contributions to this upcoming Special Issue on “Optic Neuropathies: From Molecular Mechanism to Therapy”.

Dr. Yueh Chien
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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

traumatic optic neuropathy
inherited retinal disease
Leber's hereditary optic neuropathy
retinal ganglion cell
gene delivery
cell transplantation

Published Papers (4 papers)

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Research

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25 pages, 6323 KiB

Open AccessArticle

Brief Oxygen Exposure after Traumatic Brain Injury Hastens Recovery and Promotes Adaptive Chronic Endoplasmic Reticulum Stress Responses

by Jordyn N. Torrens, Shelby M. Hetzer and Nathan K. Evanson

Int. J. Mol. Sci. 2023, 24(12), 9831; https://doi.org/10.3390/ijms24129831 - 6 Jun 2023

Cited by 1 | Viewed by 1382

Abstract

Traumatic brain injury (TBI) is a major public health concern, particularly in adolescents who have a higher mortality and incidence of visual pathway injury compared to adult patients. Likewise, we have found disparities between adult and adolescent TBI outcomes in rodents. Most interestingly, adolescents suffer a prolonged apneic period immediately post-injury, leading to higher mortality; therefore, we implemented a brief oxygen exposure paradigm to circumvent this increased mortality. Adolescent male mice experienced a closed-head weight-drop TBI and were then exposed to 100% O₂ until normal breathing returned or recovered in room air. We followed mice for 7 and 30 days and assessed their optokinetic response; retinal ganglion cell loss; axonal degeneration; glial reactivity; and retinal ER stress protein levels. O₂ reduced adolescent mortality by 40%, improved post-injury visual acuity, and reduced axonal degeneration and gliosis in optical projection regions. ER stress protein expression was altered in injured mice, and mice given O₂ utilized different ER stress pathways in a time-dependent manner. Finally, O₂ exposure may be mediating these ER stress responses through regulation of the redox-sensitive ER folding protein ERO1α, which has been linked to a reduction in the toxic effects of free radicals in other animal models of ER stress. Full article

(This article belongs to the Special Issue Optic Neuropathies: From Molecular Mechanism to Therapy)

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14 pages, 4839 KiB

Open AccessArticle

Optic Nerve Structural and Functional Changes in LHON-Affected and Asymptomatic Maternal Relatives: Association with H and HV Mitochondrial Haplogroups

by Clare Quigley, Kirk A. J. Stephenson, Paul Kenna and Lorraine Cassidy

Int. J. Mol. Sci. 2023, 24(2), 1068; https://doi.org/10.3390/ijms24021068 - 5 Jan 2023

Cited by 4 | Viewed by 1873

Abstract

Leber Hereditary Optic Neuropathy (LHON) affects a minority of carriers of causative mitochondrial DNA mutations. We investigated a cohort of patients with LHON, including m.11778G>A, m.3460G>A, m.14484T>C and DNAJC30 c.152A>G variants, and their asymptomatic maternal carrier relatives for additional potential associations with vision loss. We assessed visual acuity, optical coherence tomography (OCT) of the peripapillary retinal nerve fibre layer (RNFL), visually evoked potential including P-100 latency, and full mitochondrial genome sequencing. Comparison was made with a reference standard for OCT; European Descent, Heidelberg Engineering ©; and electrophysiology measurements with in-house normative ranges. RNFL was thinned overall in LHON patients (n = 12); median global RNFL −54 μm in the right eye (RE) and −50 μm in the left eye (LE) versus normal, and was found to be normal overall in asymptomatic carriers at +1 μm RE and −2 μm LE (n = 16). In four asymptomatic carriers there was RNFL thinning found either unilaterally or bilaterally; these cases were associated with isolated delay in P-100 latency (25%), delay and reduced visual acuity (50%), or reduced visual acuity without P-100 latency delay (25%). Optic nerve dysfunction was associated with mitochondrial haplogroup H and HV, versus non-H haplogroups, in the asymptomatic carriers (Fisher’s exact test, p = 0.05). Our findings suggest that optic nerve abnormalities may be identified in asymptomatic LHON mitochondrial mutation carriers, which may be associated with optic nerve dysfunction. For asymptomatic carriers these findings were associated with mitochondrial haplogroup H and HV. Full article

(This article belongs to the Special Issue Optic Neuropathies: From Molecular Mechanism to Therapy)

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Review

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20 pages, 665 KiB

Open AccessReview

Erythropoietin in Glaucoma: From Mechanism to Therapy

by Yi-Fen Lai, Ting-Yi Lin, Yi-Hao Chen and Da-Wen Lu

Int. J. Mol. Sci. 2023, 24(3), 2985; https://doi.org/10.3390/ijms24032985 - 3 Feb 2023

Cited by 1 | Viewed by 2313

Abstract

Glaucoma can cause irreversible vision loss and is the second leading cause of blindness worldwide. The disease mechanism is complex and various factors have been implicated in its pathogenesis, including ischemia, excessive oxidative stress, neurotropic factor deprivation, and neuron excitotoxicity. Erythropoietin (EPO) is a hormone that induces erythropoiesis in response to hypoxia. However, studies have shown that EPO also has neuroprotective effects and may be useful for rescuing apoptotic retinal ganglion cells in glaucoma. This article explores the relationship between EPO and glaucoma and summarizes preclinical experiments that have used EPO to treat glaucoma, with an aim to provide a different perspective from the current view that glaucoma is incurable. Full article

(This article belongs to the Special Issue Optic Neuropathies: From Molecular Mechanism to Therapy)

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17 pages, 813 KiB

Open AccessReview

The Latest Evidence of Erythropoietin in the Treatment of Glaucoma

by Ting-Yi Lin, Yi-Fen Lai, Yi-Hao Chen and Da-Wen Lu

Int. J. Mol. Sci. 2022, 23(24), 16038; https://doi.org/10.3390/ijms232416038 - 16 Dec 2022

Cited by 5 | Viewed by 2108

Abstract

Erythropoietin (EPO) is a circulating hormone conventionally considered to be responsible for erythropoiesis. In addition to facilitating red blood cell production, EPO has pluripotent potential, such as for cognition improvement, neurogenesis, and anti-fibrotic, anti-apoptotic, anti-oxidative, and anti-inflammatory effects. In human retinal tissues, EPO receptors (EPORs) are expressed in the photoreceptor cells, retinal pigment epithelium, and retinal ganglion cell layer. Studies have suggested its potential therapeutic effects in many neurodegenerative diseases, including glaucoma. In this review, we discuss the correlation between glaucoma and EPO, physiology and potential neuroprotective function of the EPO/EPOR system, and latest evidence for the treatment of glaucoma with EPO. Full article

(This article belongs to the Special Issue Optic Neuropathies: From Molecular Mechanism to Therapy)

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