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Biomolecules
Special Issues
Retinal Diseases: Molecular Mechanisms and Therapies
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Retinal Diseases: Molecular Mechanisms and Therapies

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Cellular Biochemistry".

Deadline for manuscript submissions: 30 June 2025 | Viewed by 1515

Special Issue Editors

Dr. Ana Raquel Santiago

E-Mail Website
Guest Editor
Coimbra Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, University of Coimbra, Coimbra, Portugal
Interests: retinal diseases; neuroprotection; neurodegeneration; neuroinflammation; neuro-immune interactions; drug delivery systems; intercellular communication; extracellular vesicles
Special Issues, Collections and Topics in MDPI journals
Dr. Raquel Boia

E-Mail Website
Guest Editor
Coimbra Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, University of Coimbra, Coimbra, Portugal
Interests: retinal diseases; retinal ganglion cells; neuroprotection; neuroregeneration; neurodegeneration; neuroinflammation; drug delivery systems

Special Issue Information

Dear Colleagues,

Retinal diseases are an important cause of ocular morbidity and visual impairment globally. In developed countries, retinal diseases are the most common cause of irreversible blindness, and in developing countries retinal diseases are the second most common cause of blindness after cataract.

Covering age-related retinal diseases to inherited retinal diseases, in this Special Issue we aim to provide a thorough understanding of the molecular mechanisms governing retinal diseases, offering insights that pave the way for innovative treatment strategies.

From the molecular pathways involved in disease progression to the latest therapeutic advancements, this Special Issue will serve as a valuable resource for researchers, clinicians, and healthcare professionals seeking a deeper comprehension of retinal disorders.

Dr. Ana Raquel Santiago
Dr. Raquel Boia
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. Biomolecules is an international peer-reviewed open access monthly 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

  • retinal diseases
  • molecular mechanisms
  • therapeutic strategies
  • vision impairment
  • gene therapy
  • retinal degeneration
  • neuroprotection
  • innovative treatments

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Further information on MDPI's Special Issue polices can be found here.

Published Papers (2 papers)

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Research

17 pages, 2583 KiB  
Article
A Neuroprotective Peptide Modulates Retinal cAMP Response Element-Binding Protein (CREB), Synapsin I (SYN1), and Growth-Associated Protein 43 (GAP43) in Rats with Silicone Oil-Induced Ocular Hypertension
by Gretchen A. Johnson, Raghu R. Krishnamoorthy, Ram H. Nagaraj and Dorota L. Stankowska
Biomolecules 2025, 15(2), 219; https://doi.org/10.3390/biom15020219 - 3 Feb 2025
Viewed by 143
Abstract
This study evaluated the neuroprotective potential of peptain-1 conjugated to a cell-penetrating peptide (CPP-P1) in an ocular hypertension model of glaucoma. Brown Norway (BN) rats were subjected to intraocular pressure (IOP) elevation via intracameral injection of silicone oil (SO), with concurrent intravitreal injections [...] Read more.
This study evaluated the neuroprotective potential of peptain-1 conjugated to a cell-penetrating peptide (CPP-P1) in an ocular hypertension model of glaucoma. Brown Norway (BN) rats were subjected to intraocular pressure (IOP) elevation via intracameral injection of silicone oil (SO), with concurrent intravitreal injections of either CPP-P1 or a vehicle. Retinal cross-sections were analyzed for markers of neuroprotection, including cAMP response element-binding protein (CREB), phosphorylated CREB (p-CREB), growth-associated protein-43 (GAP43), synapsin-1 (SYN1), and superoxide dismutase 2 (SOD2). Hematoxylin and eosin staining was used to assess retinal-layer thickness. SO-treated rats exhibited significant reductions in the thickness of the inner nuclear layer (INL, 41%, p = 0.016), inner plexiform layer (IPL, 52%, p = 0.0002), and ganglion cell layer (GCL, 57%, p = 0.001). CPP-P1 treatment mitigated these reductions, preserving INL thickness by 32% (p = 0.059), IPL by 19% (p = 0.119), and GCL by 31% (p = 0.057). Increased levels of CREB (p = 0.17) and p-CREB (p = 0.04) were observed in IOP-elevated, CPP-P1-treated retinas compared to IOP-elevated, vehicle-treated retinas. Although overall GAP43 levels were low, there was a modest increase in expression within the IPL and GCL in SO- and CPP-P1-treated retinas (p = 0.15 and p = 0.09, respectively) compared to SO- and vehicle-treated retinas. SO injection reduced SYN1 expression in both IPL and GCL (p = 0.01), whereas CPP-P1 treatment significantly increased SYN1 levels in the IPL (p = 0.03) and GCL (p = 0.002). While SOD2 expression in the GCL was minimal across all groups, a trend toward increased expression was observed in CPP-P1-treated animals (p = 0.16). The SO model was replicated with SO removal after 7 days and monitored for 21 days followed by retinal flat-mount preparation to assess retinal ganglion cell (RGC) survival. A 42% loss in RGCs (p = 0.009) was observed in SO-injected eyes, which were reduced by approximately 37% (p = 0.03) with CPP-P1 treatment. These findings suggest that CPP-P1 is a promising neuroprotective agent that promotes retinal ganglion cell survival and the preservation of other retinal neurons, potentially through enhanced CREB signaling in a rat model of SO-induced ocular hypertension. Full article
(This article belongs to the Special Issue Retinal Diseases: Molecular Mechanisms and Therapies)
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10 pages, 2979 KiB  
Article
Rotenone-Induced Optic Nerve Damage and Retinal Ganglion Cell Loss in Rats
by Yasuko Yamamoto, Takazumi Taniguchi and Atsushi Shimazaki
Biomolecules 2024, 14(9), 1047; https://doi.org/10.3390/biom14091047 - 23 Aug 2024
Viewed by 1055
Abstract
Rotenone is a mitochondrial complex I inhibitor that causes retinal degeneration. A study of a rat model of rotenone-induced retinal degeneration suggested that this model is caused by indirect postsynaptic N-methyl-D-aspartate (NMDA) stimulation triggered by oxidative stress-mediated presynaptic intracellular calcium signaling. To elucidate [...] Read more.
Rotenone is a mitochondrial complex I inhibitor that causes retinal degeneration. A study of a rat model of rotenone-induced retinal degeneration suggested that this model is caused by indirect postsynaptic N-methyl-D-aspartate (NMDA) stimulation triggered by oxidative stress-mediated presynaptic intracellular calcium signaling. To elucidate the mechanisms by which rotenone causes axonal degeneration, we investigated morphological changes in optic nerves and the change in retinal ganglion cell (RGC) number in rats. Optic nerves and retinas were collected 3 and 7 days after the intravitreal injection of rotenone. The cross-sections of the optic nerves were subjected to a morphological analysis with axon quantification. The axons and somas of RGCs were analyzed immunohistochemically in retinal flatmounts. In the optic nerve, rotenone induced axonal swelling and degeneration with the incidence of reactive gliosis. Rotenone also significantly reduced axon numbers in the optic nerve. Furthermore, rotenone caused axonal thinning, fragmentation, and beading in RGCs on flatmounts and decreased the number of RGC soma. In conclusion, the intravitreal injection of rotenone in rats induced morphological abnormities with a reduced number of optic nerve axons and RGC axons when the RGC somas were degenerated. These findings help elucidate the pathogenesis of optic neuropathy induced by mitochondrial dysfunction. Full article
(This article belongs to the Special Issue Retinal Diseases: Molecular Mechanisms and Therapies)
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