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Advances in Ischemic Retinopathies
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Advances in Ischemic Retinopathies

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 (30 September 2022) | Viewed by 1939

Special Issue Editor

Dr. Ahmed S. Ibrahim

E-Mail Website
Guest Editor
Department of Ophthalmology, Visual and Anatomical Sciences, School of Medicine, Wayne State University, 540 East Canfield, Detroit, MI 48201, USA
Interests: age-related macular degeneration; retinal; pathological ocular angiogenesis

Special Issue Information

Dear Colleagues,

In ischemic retinopathies (IRs), different etiologies lead to retinal ischemia, including a progressive decline in microvascular function due to prolonged hyperglycemia and an impairment of choroidal blood flow with drusen accumulation. These processes end up in the development of proliferative diabetic retinopathy (PDR) and age-related macular degeneration (AMD), respectively. Regardless of the type of etiology that causes inadequate perfusion to the retina, once a threshold level of ischemia has been reached, the different forms of ischemic retinopathy converge a sequela of pathological angiogenesis. Such neovascular growth is the most dangerous aspect of retinopathy, as it often causes retinal detachment followed by blindness. A key question that remains under investigation at the molecular level is how hypoxia induces a common response of switching retinal ECs from the quiescent to angiogenic phenotype across the diverse group of IRs.

This Special Issue, “Advances in ischemic retinopathies”, embarks on an integrative selection of new research topics and up-to-date review articles that identify new therapeutic approaches in the field of ischemic retinopathies.

Dr. Ahmed S. Ibrahim
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

  • ischemic retinopathies
  • proliferative diabetic retinopathy (PDR)
  • age-related macular degeneration (AMD)
  • hypoxia
  • retinal detachment

Published Papers (1 paper)

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Research

14 pages, 4046 KiB  
Article
Differential Effects of Cytopathic Hypoxia on Human Retinal Endothelial Cellular Behavior: Implication for Ischemic Retinopathies
by Shaimaa El-tanani, Thangal Yumnamcha, Lalit Pukhrambam Singh and Ahmed S. Ibrahim
Int. J. Mol. Sci. 2022, 23(8), 4274; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23084274 - 12 Apr 2022
Cited by 5 | Viewed by 1502
Abstract
Loss of barrier integrity of retinal endothelial cells (RECs) is an early feature of ischemic retinopathies (IRs), but the triggering mechanisms remain incompletely understood. Previous studies have reported mitochondrial dysfunction in several forms of IRs, which creates a cytopathic hypoxic environment where cells [...] Read more.
Loss of barrier integrity of retinal endothelial cells (RECs) is an early feature of ischemic retinopathies (IRs), but the triggering mechanisms remain incompletely understood. Previous studies have reported mitochondrial dysfunction in several forms of IRs, which creates a cytopathic hypoxic environment where cells cannot use oxygen for energy production. Nonetheless, the contribution of cytopathic hypoxia to the REC barrier failure has not been fully explored. In this study, we dissect in-depth the role of cytopathic hypoxia in impairing the barrier function of REC. We employed the electric cell-substrate impedance sensing (ECIS) technology to monitor in real-time the impedance (Z) and hence the barrier functionality of human RECs (HRECs) under cytopathic hypoxia-inducing agent, Cobalt(II) chloride (CoCl2). Furthermore, data were deconvoluted to test the effect of cytopathic hypoxia on the three key components of barrier integrity; Rb (paracellular resistance between HRECs), α (basolateral adhesion between HRECs and the extracellular matrix), and Cm (HREC membrane capacitance). Our results showed that CoCl2 decreased the Z of HRECs dose-dependently. Specifically, the Rb parameter of the HREC barrier was the parameter that declined first and most significantly by the cytopathic hypoxia-inducing agent and in a dose-dependent manner. When Rb began to fall to its minimum, other parameters of the HREC barrier, including α and Cm, were unaffected. Interestingly, the compromised effect of cytopathic hypoxia on Rb was associated with mitochondrial dysfunction but not with cytotoxicity. In conclusion, our results demonstrate distinguishable dielectric properties of HRECs under cytopathic hypoxia in which the paracellular junction between adjacent HRECs is the most vulnerable target. Such selective behavior could be utilized to screen agents or genes that maintain and strengthen the assembly of HRECs tight junction complex. Full article
(This article belongs to the Special Issue Advances in Ischemic Retinopathies)
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