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Cells
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Molecular Basis of the Macular Degeneration
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Molecular Basis of the Macular Degeneration

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

Deadline for manuscript submissions: closed (30 December 2021) | Viewed by 13508

Special Issue Editors

Prof. Dr. Vincenzo Flati

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Guest Editor
Università degli Studi dell'Aquila, Department of Biotechnological and Applied Clinical Sciences, 67100 L'Aquila, Italy
Interests: autophagy; metabolism; nutrition; signal transduction
Dr. Maccarone Rita

E-Mail Website
Guest Editor
Department of Biotechnological and Applied Clinical Sciences, Università degli Studi dell'Aquila, 67100 L'Aquila, Italy
Interests: visual system; retinal degeneration; neuroprotection; electrophysiology; macular degeneration
Special Issues, Collections and Topics in MDPI journals
Dr. Annamaria Tisi

E-Mail Website
Guest Editor
Università degli Studi dell'Aquila, Department of Biotechnological and Applied Clinical Sciences, 67100 L'Aquila, Italy
Interests: retinal degeneration; neuroscience; age-related macular degeneration; electrophysiology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Macular degeneration can be classified in early, intermediate, and advanced stages and is the leading cause of blindness in the elderly in developed countries. There are two major forms of age-related macular degeneration (AMD) that are usually distinguished as dry (or non-exudative) AMD and wet (exudative) AMD. The development of the two forms can occur independently, but patients can sometimes display features of both dry and wet AMD concomitantly.

Although several advances in the management of the disease have been made, effective cures have not yet been developed and patients are in most cases inevitably destined to blindness. For this reason, it is important to deepen the knowledge of the mechanisms underlying AMD pathogenesis. Thanks also to recent technological improvements, the investigation on the molecular basis of AMD represents an exciting field of research. It is increasingly evident that the exposure to both genetic or environmental risk factors interferes with molecular processes and induces drastic changes in the signaling pathways of the cells of the retina. Thus, targeting of these events could pave the way for the development of new therapies for AMD.

The aim of this Special Issue is to assemble original data and reviews focusing on the molecular basis of AMD. Both basic and clinical research will be considered for publication. We hope that contributions from experts in the field will result in a wide collection of papers supporting researchers working on this topic.

We look forward to your contributions.

Prof. Dr. Vincenzo Flati
Dr. Maccarone Rita
Dr. Annamaria Tisi
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

  • Neovascularization
  • Age-related macular degeneration
  • Genetic testing
  • Dry AMD
  • Wet AMD

Published Papers (2 papers)

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Review

14 pages, 1259 KiB  
Review
Regulation of Rac1 Activation in Choroidal Endothelial Cells: Insights into Mechanisms in Age-Related Macular Degeneration
by Aniket Ramshekar, Haibo Wang and M. Elizabeth Hartnett
Cells 2021, 10(9), 2414; https://doi.org/10.3390/cells10092414 - 14 Sep 2021
Cited by 7 | Viewed by 3085
Abstract
Age-related macular degeneration (AMD) is one of the leading causes of blindness worldwide. Vision loss from the neovascular form is associated with the invasion of choroidal endothelial cells into the neural retina to form vision-threatening macular neovascularization (MNV). Anti-angiogenic agents are the current [...] Read more.
Age-related macular degeneration (AMD) is one of the leading causes of blindness worldwide. Vision loss from the neovascular form is associated with the invasion of choroidal endothelial cells into the neural retina to form vision-threatening macular neovascularization (MNV). Anti-angiogenic agents are the current standard of care but are effective in only ~50% of AMD cases. The molecular mechanisms involved in invasive MNV point to the importance of regulating signaling pathways that lead to pathologic biologic outcomes. In studies testing the effects of AMD-related stresses, activation of the Rho GTPase, Rac1, was found to be important for the choroidal endothelial cell invasion into the neural retina. However, current approaches to prevent Rac1 activation are inefficient and less effective. We summarize active Rac1-mediated mechanisms that regulate choroidal endothelial cell migration. Specifically, we discuss our work regarding the role of a multidomain protein, IQ motif containing GTPase activating protein 1 (IQGAP1), in sustaining pathologic Rac1 activation and a mechanism by which active Rap1, a Ras-like GTPase, may prevent active Rac1-mediated choroidal endothelial cell migration. Full article
(This article belongs to the Special Issue Molecular Basis of the Macular Degeneration)
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21 pages, 2769 KiB  
Review
The Impact of Oxidative Stress on Blood-Retinal Barrier Physiology in Age-Related Macular Degeneration
by Annamaria Tisi, Marco Feligioni, Maurizio Passacantando, Marco Ciancaglini and Rita Maccarone
Cells 2021, 10(1), 64; https://doi.org/10.3390/cells10010064 - 04 Jan 2021
Cited by 67 | Viewed by 9344
Abstract
The blood retinal barrier (BRB) is a fundamental eye component, whose function is to select the flow of molecules from the blood to the retina and vice-versa, and its integrity allows the maintenance of a finely regulated microenvironment. The outer BRB, composed by [...] Read more.
The blood retinal barrier (BRB) is a fundamental eye component, whose function is to select the flow of molecules from the blood to the retina and vice-versa, and its integrity allows the maintenance of a finely regulated microenvironment. The outer BRB, composed by the choriocapillaris, the Bruch’s membrane, and the retinal pigment epithelium, undergoes structural and functional changes in age-related macular degeneration (AMD), the leading cause of blindness worldwide. BRB alterations lead to retinal dysfunction and neurodegeneration. Several risk factors have been associated with AMD onset in the past decades and oxidative stress is widely recognized as a key factor, even if the exact AMD pathophysiology has not been exactly elucidated yet. The present review describes the BRB physiology, the BRB changes occurring in AMD, the role of oxidative stress in AMD with a focus on the outer BRB structures. Moreover, we propose the use of cerium oxide nanoparticles as a new powerful anti-oxidant agent to combat AMD, based on the relevant existing data which demonstrated their beneficial effects in protecting the outer BRB in animal models of AMD. Full article
(This article belongs to the Special Issue Molecular Basis of the Macular Degeneration)
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