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Cells
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Retinal Disorders: Cellular Mechanisms and Targeted Therapy
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Retinal Disorders: Cellular Mechanisms and Targeted Therapy

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

Deadline for manuscript submissions: 25 April 2025 | Viewed by 2757

Special Issue Editor

Dr. Takeshi Iwata

E-Mail Website
Guest Editor
Molecular and Cellular Biology Division, National Institute of Sensory Organs, National Hospital Organization Tokyo Medical Center, 2-5-1, Higashigaoka, Meguro-Ku, Tokyo 152-8902, Japan
Interests: molecular mechanisms of retinal diseases including inherited retinal diseases; inherited glaucoma; inherited optic neuropathy; age-related macular degeneration
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Over 300 genes have been identified for inherited eye diseases and yet additional novel genes and mutations are identified every year. This is due to the improvement of whole genome sequencing, resulting from short-read to long-read genome sequencing and software analysis. These novel mutations can occasionally explain disease cause and drastically change the priority of therapeutic developments. However, for each novel disease-associated gene, molecular functional studies are required to prove its involvement in disease onset. Fortunately, in recent decades, functional studies  have significantly improved through the use of omics technologies, iPS cells, gene editing, single-cell analysis, and AI. Since the approval of the gene therapy LuxturnaThis Special Issue focuses on the molecular mechanisms of disease onset for inherited ocular diseases and the development of novel therapeutics. Diseases of interest include inherited eye diseases in the cornea, lens, retina, optic nerve, and sclera.

Dr. Takeshi Iwata
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. 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

  • inherited eye diseases
  • genome
  • omics
  • gene editing
  • iPS cells
  • animal models
  • single cell analysis
  • AI
  • epigenetics

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Published Papers (2 papers)

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Research

21 pages, 9258 KiB  
Article
Transplacental Transfer of Oxytocin and Its Impact on Neonatal Cord Blood and In Vitro Retinal Cell Activity
by Claudette O. Adegboro, Wenxiang Luo, Meha Kabra, Ryan M. McAdams, Nathaniel W. York, Ruwandi I. Wijenayake, Kiana M. Suchla, De-Ann M. Pillers and Bikash R. Pattnaik
Cells 2024, 13(20), 1735; https://doi.org/10.3390/cells13201735 - 19 Oct 2024
Viewed by 903
Abstract
The development of fetal organs can be impacted by systemic changes in maternal circulation, with the placenta playing a pivotal role in maintaining pregnancy homeostasis and nutrient exchange. In clinical obstetrics, oxytocin (OXT) is commonly used to induce labor. To explore the potential [...] Read more.
The development of fetal organs can be impacted by systemic changes in maternal circulation, with the placenta playing a pivotal role in maintaining pregnancy homeostasis and nutrient exchange. In clinical obstetrics, oxytocin (OXT) is commonly used to induce labor. To explore the potential role of OXT in the placental homeostasis of OXT, we compared OXT levels in neonatal cord blood among neonates (23–42 weeks gestation) whose mothers either received prenatal OXT or experienced spontaneous labor. Our previous research revealed that the oxytocin receptor (OXTR), essential in forming the blood–retina barrier, is expressed in the retinal pigment epithelium (RPE). We hypothesized that perinatal OXT administration might influence the development of the neural retina and its vasculature, offering therapeutic potential for retinal diseases such as retinopathy of prematurity (ROP). Plasma OXT levels were measured using a commercial OXT ELISA kit. Human fetal RPE (hfRPE) cells treated with OXT (10 µM) were assessed for gene expression via RNA sequencing, revealing 14 downregulated and 32 upregulated genes. To validate these differentially expressed genes (DEGs), hfRPE cells were exposed to OXT (0.01, 0.1, 1, or 10 µM) for 12 h, followed by RNA analysis via real-time PCR. Functional, enrichment, and network analyses (Gene Ontology term, FunRich, Cytoscape) were performed to predict the affected pathways. This translational study suggests that OXT likely crosses the placenta, altering fetal OXT concentrations. RNA sequencing identified 46 DEGs involved in vital metabolic and signaling pathways and critical cellular components. Our results indicate that the perinatal administration of OXT may affect neural retina and retinal vessel development, making OXT a potential therapeutic option for developmental eye diseases, including ROP. Full article
(This article belongs to the Special Issue Retinal Disorders: Cellular Mechanisms and Targeted Therapy)
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20 pages, 3992 KiB  
Article
Novel Small Molecules with Anti-Inflammatory and Anti-Angiogenic Activity in a Mouse Model of Oxygen-Induced Retinopathy
by Adam S. Dayoub, Eesha Acharya, Adnan Dibas, Harlan P. Jones and Suchismita Acharya
Cells 2024, 13(16), 1371; https://doi.org/10.3390/cells13161371 - 17 Aug 2024
Viewed by 1596
Abstract
Retinopathy of prematurity (ROP) has a dual-phase disease pathology; in phase 1, hyperoxia-induced vaso-obliteration occurs in the retinal vasculature due to increased oxidative stress (OS) and inflammation, followed by phase 2, where hypoxia increases the overproduction of growth factors, inducing retinal neovascularization. Toll-like [...] Read more.
Retinopathy of prematurity (ROP) has a dual-phase disease pathology; in phase 1, hyperoxia-induced vaso-obliteration occurs in the retinal vasculature due to increased oxidative stress (OS) and inflammation, followed by phase 2, where hypoxia increases the overproduction of growth factors, inducing retinal neovascularization. Toll-like receptor 2 and -4 (TLR2 and TLR4) overactivation, hyper-inflammation, macrophages, and neutrophil infiltration contribute to the developing ROP. AVR-121 and AVR-123 are novel classes of small-molecule dual inhibitors of TLR2/4 tested in a human leukemia monocytic cell line (THP-1) and cord-blood-derived mononuclear cells (CBMCs). Both compounds inhibited TLR2/4 signaling-related inflammatory cytokines in THP-1 cells and inhibited VEGF-induced neovascularization in human retinal endothelial cells (HRECs), which are hallmarks of ROP. In an oxygen-induced retinopathy (OIR) murine model, the intraperitoneal injection of AVR-123 in the hyperoxia phase (P7–P12) or a nanosuspension eyedrop of AVR-123 in the hypoxic phase (P12–P17) significantly reduced vaso-obliteration, angiogenesis, and inflammatory cytokine profiles while not inhibiting the necessary growth factor VEGF in the juvenile mouse eyes. The results are consistent with our hypothesis that targeting the dual TLR2/4 pathway will reduce inflammation, angiogenesis, and vaso-obliteration in vitro and in vivo and reduce cytotoxic immune cells. AVR-123 has the potential to be developed as a therapy for ROP. Full article
(This article belongs to the Special Issue Retinal Disorders: Cellular Mechanisms and Targeted Therapy)
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