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Visual System: From the Physiology of Vision to the Treatment...
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Visual System: From the Physiology of Vision to the Treatment of Visual Loss

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (15 April 2023) | Viewed by 4401

Special Issue Editors

Dr. Laura Baroncelli

E-Mail Website
Guest Editor
Neuroscience Institute, National Research Council (CNR), Pisa, Italy
Interests: visual cortex; neural disorders; plasticity
Dr. Enrica Strettoi

E-Mail Website
Guest Editor
Neuroscience Institute, CNR, Pisa, Italy
Interests: retina; inherited photoreceptor degeneration; inflammation; remodeling circuitry

Special Issue Information

Dear Colleagues,

Vision provides more than 80% of the information we need to perceive the world. Disorders of the eye, optic nerve, and visual cortex may cause significant vision impairment, eventually leading to blindness. There are at least 2.2 billion visually impaired people around the world, and 1 billion have a vision impairment that is either preventable or is yet to be addressed. In addition to causing a deterioration in the quality of life, visual disorders place significant economic burdens on patients, their families, and the healthcare system. The investigation of vision physiology, the exploration of pathogenetic mechanisms of visual disorders, as well as the identification of tools for early diagnosis and therapeutic intervention would provide novel fundamental knowledge in the fight against visual loss. 

This Special Issue is dedicated to recent advances in the study of the visual system, both in physiological and pathological conditions. We aim to cover past and current directions in research on the structure and function of the retina, the optic nerve, and the visual cortex, with a special focus on visual disorders and therapeutic perspectives. 

We would like to invite investigators to contribute original research as well as review articles addressing the diagnosis and management of visual disorders.

Potential topics include but are not limited to:

  • Novel insights in circuits of vision;
  • Cellular and molecular pathways of visual plasticity;
  • Classification or screening of visual disorders (retina, optic nerve, visual cortex);
  • Diagnostic tools for visual disorders;
  • Software tools for visual disorder image analysis;
  • Multimodal imaging and electrophysiological techniques for the analysis of visual disorders;
  • Novel therapeutic interventions for the visual system.

Dr. Laura Baroncelli
Dr. Enrica Strettoi
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 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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • visual system
  • retinal disorders
  • optic nerve disorders
  • neural disorders

Published Papers (2 papers)

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Research

18 pages, 5900 KiB  
Article
IKKβ Inhibition Attenuates Epithelial Mesenchymal Transition of Human Stem Cell-Derived Retinal Pigment Epithelium
by Srinivasa R. Sripathi, Ming-Wen Hu, Ravi Chakra Turaga, Rebekah Mikeasky, Ganesh Satyanarayana, Jie Cheng, Yukan Duan, Julien Maruotti, Karl J. Wahlin, Cynthia A. Berlinicke, Jiang Qian, Noriko Esumi and Donald J. Zack
Cells 2023, 12(8), 1155; https://doi.org/10.3390/cells12081155 - 13 Apr 2023
Cited by 4 | Viewed by 1871
Abstract
Epithelial-mesenchymal transition (EMT), which is well known for its role in embryonic development, malignant transformation, and tumor progression, has also been implicated in a variety of retinal diseases, including proliferative vitreoretinopathy (PVR), age-related macular degeneration (AMD), and diabetic retinopathy. EMT of the retinal [...] Read more.
Epithelial-mesenchymal transition (EMT), which is well known for its role in embryonic development, malignant transformation, and tumor progression, has also been implicated in a variety of retinal diseases, including proliferative vitreoretinopathy (PVR), age-related macular degeneration (AMD), and diabetic retinopathy. EMT of the retinal pigment epithelium (RPE), although important in the pathogenesis of these retinal conditions, is not well understood at the molecular level. We and others have shown that a variety of molecules, including the co-treatment of human stem cell-derived RPE monolayer cultures with transforming growth factor beta (TGF–β) and the inflammatory cytokine tumor necrosis factor alpha (TNF–α), can induce RPE–EMT; however, small molecule inhibitors of RPE–EMT have been less well studied. Here, we demonstrate that BAY651942, a small molecule inhibitor of nuclear factor kapa-B kinase subunit beta (IKKβ) that selectively targets NF-κB signaling, can modulate TGF–β/TNF–α-induced RPE–EMT. Next, we performed RNA-seq studies on BAY651942 treated hRPE monolayers to dissect altered biological pathways and signaling events. Further, we validated the effect of IKKβ inhibition on RPE–EMT-associated factors using a second IKKβ inhibitor, BMS345541, with RPE monolayers derived from an independent stem cell line. Our data highlights the fact that pharmacological inhibition of RPE–EMT restores RPE identity and may provide a promising approach for treating retinal diseases that involve RPE dedifferentiation and EMT. Full article
(This article belongs to the Special Issue Visual System: From the Physiology of Vision to the Treatment of Visual Loss)
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21 pages, 2435 KiB  
Article
Antioxidants Prevent the Effects of Physical Exercise on Visual Cortical Plasticity
by Gabriele Sansevero, Alan Consorti, Irene Di Marco, Eva Terzibasi Tozzini, Alessandro Cellerino and Alessandro Sale
Cells 2023, 12(1), 48; https://doi.org/10.3390/cells12010048 - 22 Dec 2022
Cited by 1 | Viewed by 1848
Abstract
Background: Physical activity has been recently shown to enhance adult visual cortical plasticity, both in human subjects and animal models. While physical activity activates mitochondrial oxidative metabolism leading to a transient production of reactive oxygen species, it remains unknown whether this process is [...] Read more.
Background: Physical activity has been recently shown to enhance adult visual cortical plasticity, both in human subjects and animal models. While physical activity activates mitochondrial oxidative metabolism leading to a transient production of reactive oxygen species, it remains unknown whether this process is involved in the plasticizing effects elicited at the visual cortical level. Results: Here, we investigated whether counteracting oxidative stress through a dietary intervention with antioxidants (vitamins E and C) interferes with the impact of physical exercise on visual cortex plasticity in adult rats. Antioxidant supplementation beyond the closure of the critical period blocked ocular dominance plasticity in response to eye deprivation induced by physical activity in adult rats. Conclusions: Antioxidants exerted their action through a mithormetic effect that involved dampening of oxidative stress and insulin-like growth factor 1 (IGF-1) signaling in the brain. Full article
(This article belongs to the Special Issue Visual System: From the Physiology of Vision to the Treatment of Visual Loss)
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