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Special Issue "Retina Degeneration, Neuroprotection and Repair"

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

Deadline for manuscript submissions: 30 June 2021.

Special Issue Editors

Dr. Arturo Ortín-Martínez
E-Mail Website
Guest Editor
Donald K. Johnson Eye Institute, Krembil Research Institute, University Health Network, Toronto, Canada
Interests: retina; photoreceptors; retinal ganglion cells; degeneration; neuroprotection; regenerative medicine; cell therapy; macular degeneration; retinitis pigmentosa; glaucoma
Dr. Luis Alarcon-Martinez
E-Mail
Guest Editor
University of Montreal Hospital Research Center (CRCHUM), Montreal, Canada
Interests: retina; vascular system; neurovascular coupling; pericytes; functional hyperaemia; electroretinography; two-photon microscopy
Dr. Sandra Petrus-Reurer
E-Mail
Guest Editor
University of Cambridge, Cambridge, United Kingdom
Interests: retina; retinal pigment epithelial cells; human embryonic stem cells; RPE differentiation; cellular repair; retinal progenitor; preclinical animal model; macular degeneration; immunology of allorejection; immunomodulation

Special Issue Information

Dear Colleagues,

We are pleased to announce the upcoming Special Issue “Retina Neurodegeneration, Neuroprotection and Repair”.

Globally, 1.2 billion people live with blindness or a vision impairment that could not be prevented or addressed. Age-related macular degeneration (170 million), glaucoma (7 million), diabetic retinopathy (3 million), and retinitis pigmentosa (1.5 million) are some of the main pathologies leading to irreversible visual impairment and blindness.

The capacity for endogenous repair is effectively absent in the mammalian central nervous system, including the retina, which exhibits no intrinsic regenerative capacities; therefore, retinal degenerative diseases such as those listed above result in permanent and irreversible impairment.

Currently, great scientific efforts are focused on bringing sight and a better understanding of: i) the mechanisms that lead to the degeneration of key retinal cell populations such as photoreceptors and retinal ganglion cells; ii) the neuroinflammatory response that accompanied the degeneration, involving retinal microglia cells and inflammatory mediators; iii) circulatory blood flow implications in the progression of the neurodegenerative process; iv) identification of new molecular targets to delay or impede the progression of the degeneration; v) regenerative medicine approaches such as gene therapy and cell replacement strategies to restore function loss.

This Special Issue shall cover results of studies using experimental models (animal or cell culture models) to investigate the mechanism of progression of retina degeneration and cell death, strategies to stop or delay the progression, including neuroprotective pharmaceutical target and/or therapeutic approaches based on regenerative medicine such as gene and cell therapy, to restore vision. 

We warmly welcome short communications, original research articles, and review articles for this Special Issue.

Dr. Arturo Ortín-Martínez
Dr. Luis Alarcón-Martínez
Dr. Sandra Petrus-Reurer
Guest Editors

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 papers will be 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

  • retina
  • age-related macular degeneration
  • retinitis pigmentosa
  • glaucoma
  • photoreceptors
  • retinal ganglion cells
  • degeneration
  • neuroprotection
  • neuroinflammation
  • retina blood flow
  • regenerative medicine
  • gene therapy
  • transplantation
  • cell therapy

Published Papers (1 paper)

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Research

Open AccessArticle
Retinal Molecular Changes Are Associated with Neuroinflammation and Loss of RGCs in an Experimental Model of Glaucoma
Int. J. Mol. Sci. 2021, 22(4), 2066; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22042066 - 19 Feb 2021
Viewed by 643
Abstract
Signaling mediated by cytokines and chemokines is involved in glaucoma-associated neuroinflammation and in the damage of retinal ganglion cells (RGCs). Using multiplexed immunoassay and immunohistochemical techniques in a glaucoma mouse model at different time points after ocular hypertension (OHT), we analyzed (i) the [...] Read more.
Signaling mediated by cytokines and chemokines is involved in glaucoma-associated neuroinflammation and in the damage of retinal ganglion cells (RGCs). Using multiplexed immunoassay and immunohistochemical techniques in a glaucoma mouse model at different time points after ocular hypertension (OHT), we analyzed (i) the expression of pro-inflammatory cytokines, anti-inflammatory cytokines, BDNF, VEGF, and fractalkine; and (ii) the number of Brn3a+ RGCs. In OHT eyes, there was an upregulation of (i) IFN-γ at days 3, 5, and 15; (ii) IL-4 at days 1, 3, 5, and 7 and IL-10 at days 3 and 5 (coinciding with downregulation of IL1-β at days 1, 5, and 7); (iii) IL-6 at days 1, 3, and 5; (iv) fractalkine and VEGF at day 1; and (v) BDNF at days 1, 3, 7, and 15. In contralateral eyes, there were (i) an upregulation of IL-1β at days 1 and 3 and a downregulation at day 7, coinciding with the downregulation of IL4 at days 3 and 5 and the upregulation at day 7; (ii) an upregulation of IL-6 at days 1, 5, and 7 and a downregulation at 15 days; (iii) an upregulation of IL-10 at days 3 and 7; and (iv) an upregulation of IL-17 at day 15. In OHT eyes, there was a reduction in the Brn3a+ RGCs number at days 3, 5, 7, and 15. OHT changes cytokine levels in both OHT and contralateral eyes at different time points after OHT induction, confirming the immune system involvement in glaucomatous neurodegeneration. Full article
(This article belongs to the Special Issue Retina Degeneration, Neuroprotection and Repair)
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