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Advances in Ocular Pharmacology and Therapeutics
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Advances in Ocular Pharmacology and Therapeutics

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 (15 July 2023) | Viewed by 11455

Special Issue Editor

Dr. Simon Kaja

E-Mail Website1 Website2
Guest Editor
Department of Ophthalmology, Loyola University Chicago, Stritch School of Medicine, Maywood, IL 60153, USA
Interests: ophthalmic drugs; dry eye disease; ocular surface disease; drug delivery; ocular pharmacology; ocular toxicology; glaucoma; antioxidants; angiogenesis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Vision impairment and vision loss associated with age-related ocular diseases pose a significant economic and societal impact worldwide and account for a significant decline in workplace productivity and quality of life. Major age-related ocular diseases include age-related macular degeneration, diabetic retinopathy, and glaucoma and collectively represent an urgent and unmet clinical necessity to develop novel safe and efficacious therapeutics that can slow or halt the progression of disease.

In this Special Issue of IJMS, we are seeking articles that investigate the underlying molecular mechanisms of ocular disease and describe advances in molecular pharmacology related to ophthalmic indications.

We are particularly interested in molecular studies in animal models of ocular disease, including but not limited to age-related macular degeneration, diabetic retinopathy, dry eye disease, and glaucoma. Studies that utilize non-rodent models for ocular disease are particularly encouraged. Unfortunately, purely clinical studies are beyond the scope of this Special Issue.

Dr. Simon Kaja
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

  • pathophysiology
  • treatment
  • animal model
  • glaucoma
  • macular degeneration
  • diabetic retinopathy
  • dry eye disease
  • pharmacology
  • therapeutics
  • vision loss
  • blindness
  • neurodegeneration

Published Papers (4 papers)

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Research

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18 pages, 4175 KiB  
Article
Regional Gene Expression in the Retina, Optic Nerve Head, and Optic Nerve of Mice with Optic Nerve Crush and Experimental Glaucoma
by Casey J. Keuthan, Julie A. Schaub, Meihan Wei, Weixiang Fang, Sarah Quillen, Elizabeth Kimball, Thomas V. Johnson, Hongkai Ji, Donald J. Zack and Harry A. Quigley
Int. J. Mol. Sci. 2023, 24(18), 13719; https://doi.org/10.3390/ijms241813719 - 6 Sep 2023
Cited by 4 | Viewed by 1618
Abstract
A major risk factor for glaucomatous optic neuropathy is the level of intraocular pressure (IOP), which can lead to retinal ganglion cell axon injury and cell death. The optic nerve has a rostral unmyelinated portion at the optic nerve head followed by a [...] Read more.
A major risk factor for glaucomatous optic neuropathy is the level of intraocular pressure (IOP), which can lead to retinal ganglion cell axon injury and cell death. The optic nerve has a rostral unmyelinated portion at the optic nerve head followed by a caudal myelinated region. The unmyelinated region is differentially susceptible to IOP-induced damage in rodent models and human glaucoma. While several studies have analyzed gene expression changes in the mouse optic nerve following optic nerve injury, few were designed to consider the regional gene expression differences that exist between these distinct areas. We performed bulk RNA-sequencing on the retina and separately micro-dissected unmyelinated and myelinated optic nerve regions from naïve C57BL/6 mice, mice after optic nerve crush, and mice with microbead-induced experimental glaucoma (total = 36). Gene expression patterns in the naïve unmyelinated optic nerve showed significant enrichment of the Wnt, Hippo, PI3K-Akt, and transforming growth factor β pathways, as well as extracellular matrix–receptor and cell membrane signaling pathways, compared to the myelinated optic nerve and retina. Gene expression changes induced by both injuries were more extensive in the myelinated optic nerve than the unmyelinated region, and greater after nerve crush than glaucoma. Changes present three and fourteen days after injury largely subsided by six weeks. Gene markers of reactive astrocytes did not consistently differ between injury states. Overall, the transcriptomic phenotype of the mouse unmyelinated optic nerve was significantly different from immediately adjacent tissues, likely dominated by expression in astrocytes, whose junctional complexes are inherently important in responding to IOP elevation. Full article
(This article belongs to the Special Issue Advances in Ocular Pharmacology and Therapeutics)
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14 pages, 3698 KiB  
Article
Regulation of Aqueous Humor Secretion by Melatonin in Porcine Ciliary Epithelium
by Ka-Lok Li, Sze-Wan Shan, Fang-Yu Lin, Choi-Ying Ling, Nga-Wai Wong, Hoi-Lam Li, Wei Han, Chi-Ho To and Chi-Wai Do
Int. J. Mol. Sci. 2023, 24(6), 5789; https://doi.org/10.3390/ijms24065789 - 17 Mar 2023
Cited by 1 | Viewed by 1523
Abstract
Secretion of melatonin, a natural hormone whose receptors are present in the ciliary epithelium, displays diurnal variation in the aqueous humor (AH), potentially contributing to the regulation of intraocular pressure. This study aimed to determine the effects of melatonin on AH secretion in [...] Read more.
Secretion of melatonin, a natural hormone whose receptors are present in the ciliary epithelium, displays diurnal variation in the aqueous humor (AH), potentially contributing to the regulation of intraocular pressure. This study aimed to determine the effects of melatonin on AH secretion in porcine ciliary epithelium. The addition of 100 µM melatonin to both sides of the epithelium significantly increased the short-circuit current (Isc) by ~40%. Stromal administration alone had no effect on the Isc, but aqueous application triggered a 40% increase in Isc, similar to that of bilateral application without additive effect. Pre-treatment with niflumic acid abolished melatonin-induced Isc stimulation. More importantly, melatonin stimulated the fluid secretion across the intact ciliary epithelium by ~80% and elicited a sustained increase (~50–60%) in gap junctional permeability between pigmented ciliary epithelial (PE) cells and non-pigmented ciliary epithelial (NPE) cells. The expression of MT3 receptor was found to be >10-fold higher than that of MT1 and MT2 in porcine ciliary epithelium. Aqueous pre-treatment with MT1/MT2 antagonist luzindole failed to inhibit the melatonin-induced Isc response, while MT3 antagonist prazosin pre-treatment abolished the Isc stimulation. We conclude that melatonin facilitates Cl− and fluid movement from PE to NPE cells, thereby stimulating AH secretion via NPE-cell MT3 receptors. Full article
(This article belongs to the Special Issue Advances in Ocular Pharmacology and Therapeutics)
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13 pages, 3766 KiB  
Article
Activation of ADRB2/PKA Signaling Pathway Facilitates Lipid Synthesis in Meibocytes, and Beta-Blocker Glaucoma Drug Impedes PKA-Induced Lipid Synthesis by Inhibiting ADRB2
by Ikhyun Jun, Young Joon Choi, Bo-Rahm Kim, Kyoung Yul Seo and Tae-im Kim
Int. J. Mol. Sci. 2022, 23(16), 9478; https://doi.org/10.3390/ijms23169478 - 22 Aug 2022
Cited by 6 | Viewed by 2317
Abstract
Meibomian gland dysfunction is one of the main causes of dry eye disease and has limited therapeutic options. In this study, we investigated the biological function of the beta 2-adrenergic receptor (ADRB2)/protein kinase A (PKA) pathway in lipid synthesis and its underlying mechanisms [...] Read more.
Meibomian gland dysfunction is one of the main causes of dry eye disease and has limited therapeutic options. In this study, we investigated the biological function of the beta 2-adrenergic receptor (ADRB2)/protein kinase A (PKA) pathway in lipid synthesis and its underlying mechanisms in human meibomian gland epithelial cells (HMGECs). HMGECs were cultured in differentiation media with or without forskolin (an activator of adenylate cyclase), salbutamol (an ADRB2 agonist), or timolol (an ADRB2 antagonist) for up to 4 days. The phosphorylation of the cAMP-response element-binding protein (CREB) and the expression of peroxisome proliferator activator receptor (PPAR)γ and sterol regulatory element-binding protein (SREBP)-1 were measured by immunoblotting and quantitative PCR. Lipid synthesis was examined by LipidTOX immunostaining, AdipoRed assay, and Oil Red O staining. PKA pathway activation enhanced PPARγ expression and lipid synthesis in differentiated HMGECs. When treated with agonists of ADBR2 (upstream of the PKA signaling system), PPARγ expression and lipid synthesis were enhanced in HMGECs. The ADRB2 antagonist timolol showed the opposite effect. The activation of the ADRB2/PKA signaling pathway enhances lipid synthesis in HMGECs. These results provide a potential mechanism and therapeutic target for meibomian gland dysfunction, particularly in cases induced by beta-blocker glaucoma drugs. Full article
(This article belongs to the Special Issue Advances in Ocular Pharmacology and Therapeutics)
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Review

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23 pages, 817 KiB  
Review
The Role of Citicoline and Coenzyme Q10 in Retinal Pathology
by Claudia García-López, Verónica García-López, José A. Matamoros, José A. Fernández-Albarral, Elena Salobrar-García, Rosa de Hoz, Inés López-Cuenca, Lidia Sánchez-Puebla, José M. Ramírez, Ana I. Ramírez and Juan J. Salazar
Int. J. Mol. Sci. 2023, 24(6), 5072; https://doi.org/10.3390/ijms24065072 - 7 Mar 2023
Cited by 2 | Viewed by 5499
Abstract
Ocular neurodegenerative diseases such as glaucoma, diabetic retinopathy, and age-related macular degeneration are common retinal diseases responsible for most of the blindness causes in the working-age and elderly populations in developed countries. Many of the current treatments used in these pathologies fail to [...] Read more.
Ocular neurodegenerative diseases such as glaucoma, diabetic retinopathy, and age-related macular degeneration are common retinal diseases responsible for most of the blindness causes in the working-age and elderly populations in developed countries. Many of the current treatments used in these pathologies fail to stop or slow the progression of the disease. Therefore, other types of treatments with neuroprotective characteristics may be necessary to allow a more satisfactory management of the disease. Citicoline and coenzyme Q10 are molecules that have neuroprotective, antioxidant, and anti-inflammatory properties, and their use could have a beneficial effect in ocular neurodegenerative pathologies. This review provides a compilation, mainly from the last 10 years, of the main studies that have been published on the use of these drugs in these neurodegenerative diseases of the retina, analyzing the usefulness of these drugs in these pathologies. Full article
(This article belongs to the Special Issue Advances in Ocular Pharmacology and Therapeutics)
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