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Mechanism of Cell Signaling During Eye Development and Diseases—Second Edition
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Mechanism of Cell Signaling During Eye Development and Diseases—Second Edition

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

Deadline for manuscript submissions: 20 October 2025 | Viewed by 3522

Special Issue Editors

Dr. Mehrnoosh Saghizadeh Ghiam

E-Mail Website
Guest Editor
Board of Governors Regenerative Medicine Institute, Eye Program, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA
Interests: diabetic cornea; limbal stem cells; microRNA; extracellular vesicles/exosomes; wound healing; gene therapy; stem cell therapy; corneal epithelial regeneration; intercellular communication
Special Issues, Collections and Topics in MDPI journals
Dr. Vivien Coulson-Thomas

E-Mail Website
Guest Editor
The Ocular Surface Institute (TOSI), College of Optometry, University of Houston, Health and Biomedical Sciences Building, Houston, TX, USA
Interests: extracellular matrix; corneal development and wound healing; limbal stem cells; stem cell therapy; corneal regeneration; dry eye disease; meibomian gland dysfunction
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This is the expanded second edition of the Special Issue “Mechanism of Cell Signaling During Eye Development and Diseases”. Previous articles published in the 1st edition can be read by clicking the following link: https://www.mdpi.com/journal/cells/special_issues/UCD4H97HG7.

Cell signaling pathways are important in mediating essential processes in embryonic eye development and adult tissues. Their coordination and integration are critical for mediating processes ranging from cell proliferation and differentiation to cell fate determination and polarity. Cellular communication is compelled by these pathways and is driven by hormones, transcription factors, or other signaling molecules.

Several major signaling pathways in eye development, such as Hedgehog, Wnt, retinoic acid, FGF, TGF-β, and Notch, operate during development in a precise temporal and spatial patterning in the embryo and in adult tissues, generating diverse cellular responses in a cell-type-specific manner. Altered expressions of these pathways can lead to a large number of eye diseases, such as photoreceptor degeneration as a result of a dysregulated Wnt signaling pathway, Glaucoma as a result of altered TGF-β signaling, and pathological angiogenesis-related eye disorders due to defects in Notch signaling.

Therefore, delineating the mechanisms of cell signaling during eye development and disease can unveil their potential as targets for novel therapeutic strategies for the treatment of ocular diseases.

Dr. Mehrnoosh Saghizadeh Ghiam
Dr. Vivien Coulson-Thomas
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

  • cell signaling
  • ocular
  • eye disorders
  • Wnt signaling
  • TGF-β

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Published Papers (4 papers)

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Research

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16 pages, 3663 KB  
Article
Impact of Donor and Host Age on Systemic Cell Therapy to Treat Age-Related Macular Degeneration
by Carolina Francelin, Xiaoping Qi, Juliana Godoy, Brenton T. Bicknell, Ram Prasad, Maria B. Grant and Michael E. Boulton
Cells 2025, 14(17), 1360; https://doi.org/10.3390/cells14171360 - 1 Sep 2025
Viewed by 590
Abstract
Purpose: We previously reported that the systemic administration of preprogrammed mouse hematopoietic bone marrow-derived progenitor cells (HSPCs) improved visual function and restored a functional retinal pigment epithelial (RPE) layer. Here, we investigated the potential impact of donor vs. host age on systemic cellular [...] Read more.
Purpose: We previously reported that the systemic administration of preprogrammed mouse hematopoietic bone marrow-derived progenitor cells (HSPCs) improved visual function and restored a functional retinal pigment epithelial (RPE) layer. Here, we investigated the potential impact of donor vs. host age on systemic cellular therapy in a murine model of retinal degeneration. Methods: HSPCs from young (8 weeks) and old (15 months) mice were programmed ex vivo with a lentiviral vector expressing the RPE65 gene (LV-RPE65) and systemically administering into young or old SOD2 KD mice. Visual loss and pathological changes were evaluated by electroretinogram (ERG), optical coherence tomography (OCT), histology, and immunohistochemistry. Results: Old donor HSPCs administered to old manganese superoxide dismutase (SOD2) knockdown (KD) recipient mice offered the least benefit. This was exemplified by the reduced recruitment and incorporation of LV-RPE65 HSPC into the RPE layer, as well as decreased improvement in visual function, retinal thinning, and limited reduction in oxidative damage and microglial activation. LV-RPE65 HSPC from young mice incorporated into the RPE layer of old SOD2 KD mice, though to a lesser extent than young cells administered to young hosts, offered some level of protection. By contrast, LV-RPE65 HSPCs from old mice, located to the subretinal space of young host mice, reduced visual loss, although some retinal pathology was observed. Conclusions: The administration of LV-RPE65 HSPC from old donors to old SOD2 KD mice offered the least improvement. Translational Relevance: Our findings highlight how both donor and recipient age impact the success of HSPC-based retinal therapy and using cells from aged donors for AMD treatment may have some limitations. Full article
(This article belongs to the Special Issue Mechanism of Cell Signaling During Eye Development and Diseases—Second Edition)
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18 pages, 3328 KB  
Article
Targeting Diabetic Retinopathy with Human iPSC-Derived Vascular Reparative Cells in a Type 2 Diabetes Model
by Sergio Li Calzi, Dibyendu Chakraborty, Ping Hu, Ram Prasad, Yvonne Adu-Rutledge, Cristiano Vieira, Fadeela Sheini, Michael E. Boulton, Mervin C. Yoder, Changde Cheng and Maria B. Grant
Cells 2025, 14(17), 1352; https://doi.org/10.3390/cells14171352 - 30 Aug 2025
Viewed by 572
Abstract
Purpose: To investigate the therapeutic potential of inducible pluripotent stem cell (hiPSC)-based vascular repair, we evaluated two vascular reparative cell populations, CD34+ cells derived from hiPSC (hiPSC-CD34+) and endothelial colony forming cells (ECFCs) derived from hiPSC (iPS-ECFCs), alone and in [...] Read more.
Purpose: To investigate the therapeutic potential of inducible pluripotent stem cell (hiPSC)-based vascular repair, we evaluated two vascular reparative cell populations, CD34+ cells derived from hiPSC (hiPSC-CD34+) and endothelial colony forming cells (ECFCs) derived from hiPSC (iPS-ECFCs), alone and in combination, in a type 2 diabetic (db/db) mouse model of DR. Methods: hiPSC-CD34+ cells (1 × 104) or iPSC- ECFCs (1 × 105) alone or in combination (1.1 × 105) were injected into the vitreous of immunosuppressed db/db mice with six months of established diabetes. One month post-injection, mice underwent electroretinography (ERG) and optical coherence tomography (OCT) to evaluate functional and structural retinal recovery with iPSC administration. Immunohistochemistry (IHC) was used to assess recruitment and incorporation of cells into the retinal vasculature. Retinas from the experimental groups were analyzed using Functional Proteomics via Reverse Phase Protein Array (RPPA). Results: Functional assessment via ERG demonstrated significant improvements in retinal response in the diabetic cohorts treated with either hiPSC-derived CD34+ cells or hiPSC-ECFCs. Retinal thickness, assessed by OCT, was restored to near-nondiabetic levels in mice treated with hiPSC-CD34+ cells alone and the combination group, whereas hiPSC-ECFCs alone did not significantly affect retinal thickness. One month following intravitreal injection, hiPSC-CD34+ cells were localized to perivascular regions, whereas hiPSC-ECFCs were observed to integrate directly into the retinal vasculature. RPPA analysis revealed interaction-significant changes, and this was interpreted as a combination-specific, non-additive host responses (m6A, PI3K–AKT–mTOR, glycolysis, endothelial junction pathways). Conclusions: The studies support that injection of hiPSC-CD34+ cells and hiPSC-ECFCs, both individually and in combination, showed benefit; however, iPSC combination-specific effects were identified by measurement of retinal thickness and by RPPA. Full article
(This article belongs to the Special Issue Mechanism of Cell Signaling During Eye Development and Diseases—Second Edition)
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Review

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30 pages, 937 KB  
Review
Mechanisms of Corneal Nerve Regeneration: Examining Molecular Regulators
by Bianca Bigit, Victor H. Guaiquil, Ali R. Djalilian and Mark I. Rosenblatt
Cells 2025, 14(17), 1322; https://doi.org/10.3390/cells14171322 - 27 Aug 2025
Viewed by 613
Abstract
Corneal nerve integrity is vital for maintaining ocular surface health and visual clarity, but damage from injury or disease can lead to pain, persistent epithelial defects, and even vision loss. A deeper understanding of how corneal nerves regenerate at the molecular level is [...] Read more.
Corneal nerve integrity is vital for maintaining ocular surface health and visual clarity, but damage from injury or disease can lead to pain, persistent epithelial defects, and even vision loss. A deeper understanding of how corneal nerves regenerate at the molecular level is key to developing therapies that restore both anatomical structure and function. In this review, we bring together current insights into the pathways that drive corneal nerve repair after injury. We outline the major signaling pathways that promote neuronal survival, axon extension, and nerve–epithelial interactions, along with evolving research around novel modulators that could improve repair outcomes. Although advances in imaging and molecular therapies have led to significant progress in promoting nerve regrowth, functional sensory recovery often lags. This gap in recovery emphasizes the need for research approaches that align anatomical restoration with sensory function. In this review, we aim to clarify the mechanisms underlying corneal nerve regeneration (and their intersections) and identify opportunities for improving patient outcomes. Full article
(This article belongs to the Special Issue Mechanism of Cell Signaling During Eye Development and Diseases—Second Edition)
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26 pages, 6136 KB  
Review
Exosomes as Future Therapeutic Tools and Targets for Corneal Diseases
by Joshua Gamez, Daxian Zha, Shaghaiegh M. Ebrahimi, Seok White, Alexander V. Ljubimov and Mehrnoosh Saghizadeh
Cells 2025, 14(13), 959; https://doi.org/10.3390/cells14130959 - 23 Jun 2025
Viewed by 1330
Abstract
The therapeutic potential of exosomes (Exos), a subpopulation of extracellular vesicles (EVs) secreted by various cell types, has been broadly emphasized. Exos are endosome-derived membrane-bound vesicles 50–150 nm in size. Exos can be general or cell type-specific. Their contents enable them to function [...] Read more.
The therapeutic potential of exosomes (Exos), a subpopulation of extracellular vesicles (EVs) secreted by various cell types, has been broadly emphasized. Exos are endosome-derived membrane-bound vesicles 50–150 nm in size. Exos can be general or cell type-specific. Their contents enable them to function as multi-signaling and vectorized vehicles. Exos are important for maintaining cellular homeostasis. They are released into extracellular spaces, leading to uptake by neighboring or distant cells and delivering their contents to modulate cell signaling. Exos influence tissue responses to injury, infection, and disease by fusion with the target cells and transferring their cargo, including cytokines, growth and angiogenic factors, signaling molecules, lipids, DNA, mRNAs, and non-coding RNAs. They are implicated in various physiological and pathological conditions, including ocular surface events, such as corneal scarring, wound healing, and inflammation. Their biocompatibility, stability, low immunogenicity, and easy detectability in bodily fluids (blood, tears, saliva, and urine) make them promising tools for diagnosing and treating ocular diseases. The potential to engineer specific Exo cargos makes them outstanding therapeutic delivery vehicles. The objective of this review is to provide novel insights into the functions of Exo cargos and their applications as biomarkers and therapeutics, or targets in the cornea. Full article
(This article belongs to the Special Issue Mechanism of Cell Signaling During Eye Development and Diseases—Second Edition)
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