Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
9.0
4.9
Journals
IJMS
Special Issues
Molecular and Cellular Mechanisms of Retinal Diseases
ijms-logo
Submit to Special Issue Submit Abstract to Special Issue Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Molecular and Cellular Mechanisms of Retinal Diseases

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: 30 October 2025 | Viewed by 3190

Special Issue Editor

Dr. Maria Consiglia Trotta

E-Mail Website
Guest Editor
Department of Experimental Medicine, University of Campania “Luigi Vanvitelli”, 80138 Naples, Italy
Interests: diabetic retinopathy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are pleased to announce the call for submissions to our upcoming Special Issue titled “Molecular and Cellular Mechanisms of Retinal Diseases”. This describes severe ophthalmic complications affecting the retina and one of the leading causes of vision loss in patients. Although several tests for retinopathy diagnosis and different therapeutic options are currently available to treat or prevent the development of retinal diseases, their management remains challenging.

Given the significant impact of retinopathies on public health, especially considering diabetic retinopathy, there is an urgent need for novel comprehensive research to understand the cellular and molecular mechanisms underlying their pathophysiology to identify novel therapeutic targets for modulation, thus improving overall patient outcomes.

By shedding light on novel cellular and molecular pathways potentially involved in the development of neuronal and mitochondrial dysfunction, inflammation, oxidative stress, fibrosis, and vascular abnormalities in diabetic retina, this Special Issue will provide new insights and discoveries through research on retinal diseases by suggesting the modulation of specific cellular and molecular retinal targets as new preventive or therapeutic strategies to improve retinopathy management.

This Special Issue will consider original research and review articles on new scientific developments related to the cellular and molecular mechanisms implicated in the prevention, progression, and resolution of retinal diseases.

Dr. Maria Consiglia Trotta
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

  • retinopathies
  • diabetic retinopathy
  • inflammation
  • pro-resolving mediators
  • fibrosis
  • epithelial–mesenchymal transition
  • microRNAs

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

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

Published Papers (3 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

23 pages, 4417 KiB  
Article
Hypoxia-Dependent Upregulation of VEGF Relies on β3-Adrenoceptor Signaling in Human Retinal Endothelial and Müller Cells
by Martina Lucchesi, Lorenza Di Marsico, Lorenzo Guidotti, Matteo Lulli, Luca Filippi, Silvia Marracci and Massimo Dal Monte
Int. J. Mol. Sci. 2025, 26(9), 4043; https://doi.org/10.3390/ijms26094043 - 24 Apr 2025
Viewed by 367
Abstract
β-adrenoceptors (BARs) are involved in vascular endothelial growth factor (VEGF) production during retinal neovascularization. Here, using human retinal endothelial and Müller cells (hRECs and MIO-M1, respectively), we evaluated the effects exerted by hypoxia on BARs, hypoxia-inducible factor-1α subunit (HIF-1α) and VEGF, as well [...] Read more.
β-adrenoceptors (BARs) are involved in vascular endothelial growth factor (VEGF) production during retinal neovascularization. Here, using human retinal endothelial and Müller cells (hRECs and MIO-M1, respectively), we evaluated the effects exerted by hypoxia on BARs, hypoxia-inducible factor-1α subunit (HIF-1α) and VEGF, as well as the involvement of BAR3 and nitric oxide synthase (NOS) enzymes in hypoxia-induced VEGF production. We altered oxygen availability through a hypoxic incubator. BARs, HIF-1 α and VEGF levels were evaluated. Cells were treated with the BAR3 antagonist SR59230A, different NOS inhibitors or the NO donor SNAP. The influence of the BAR3/NOS axis on hypoxic VEGF production was assessed. Hypoxia upregulated BAR3, HIF-1α and VEGF in hRECs and MIO-M1 cells. SR59230A counteracted hypoxia-dependent VEGF increase in both cell lines, exerting no effect on HIF-1α upregulation. Treatments with NOS inhibitors prevented the hypoxia-dependent VEGF increase, while SNAP abrogated the effect of SR59230A in reducing hypoxia-induced VEGF upregulation. The present results corroborate the hypothesis that in the hypoxic retina, BAR3 influence on VEGF production is mediated by NO and suggest that, at least in endothelial and Müller cells, BAR3 activity is necessary to allow the HIF-1-mediated VEGF upregulation. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Retinal Diseases)
►▼ Show Figures

Figure 1

17 pages, 4297 KiB  
Article
Citrulline Plus Arginine Induces an Angiogenic Response and Increases Permeability in Retinal Endothelial Cells via Nitric Oxide Production
by Cassandra Warden, Daniella Zubieta and Milam A. Brantley, Jr.
Int. J. Mol. Sci. 2025, 26(5), 2080; https://doi.org/10.3390/ijms26052080 - 27 Feb 2025
Viewed by 730
Abstract
We previously observed elevated plasma levels of citrulline and arginine in diabetic retinopathy patients compared to diabetic controls. We tested our hypothesis that citrulline plus arginine induces angiogenesis and increases permeability in retinal endothelial cells. Human retinal microvascular endothelial cells (HRMECs) were treated [...] Read more.
We previously observed elevated plasma levels of citrulline and arginine in diabetic retinopathy patients compared to diabetic controls. We tested our hypothesis that citrulline plus arginine induces angiogenesis and increases permeability in retinal endothelial cells. Human retinal microvascular endothelial cells (HRMECs) were treated with citrulline, arginine, or citrulline + arginine, and angiogenesis was measured with cell proliferation, migration, and tube formation assays. Permeability was measured in HRMEC monolayers via trans-endothelial electrical resistance (TEER) and FITC-labeled dextran. We also measured arginase activity, arginase-1 and arginase-2 expression, protein expression and phosphorylation of endothelial nitric oxide synthase (eNOS), and nitric oxide (NO) production. Citrulline + arginine induced endothelial cell proliferation (p = 0.018), migration (p = 0.011), and tube formation (p = 0.0042). Citrulline + arginine also increased FITC-dextran flow-through (p = 1.5 × 10−5) and decreased TEER (p = 0.010). Citrulline + arginine had no effect on arginase activity, but it increased eNOS (p = 6.3 × 10−4) and phosphorylated eNOS (p = 0.029), as well as NO production (p = 0.025). Inhibiting eNOS prevented the increase in NO (p = 0.0092), inhibited citrulline + arginine-induced cell migration (p = 0.0080) and tube formation (p = 0.0092), and blocked citrulline + arginine-related alterations in FITC-dextran flow-through (p = 3.6 × 10−4) and TEER (p = 3.9 × 10−4). These data suggest that citrulline + arginine treatment induces angiogenesis and increases permeability in retinal endothelial cells by activating eNOS and increasing NO production. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Retinal Diseases)
►▼ Show Figures

Figure 1

13 pages, 2529 KiB  
Article
Optimal Humanized Scg3-Neutralizing Antibodies for Anti-Angiogenic Therapy of Diabetic Retinopathy
by Chengchi Huang, Prabuddha Waduge, Avinash Kaur, Hong Tian, Christina Y. Weng, John Timothy Stout, Iok-Hou Pang, Keith A. Webster and Wei Li
Int. J. Mol. Sci. 2024, 25(17), 9507; https://doi.org/10.3390/ijms25179507 - 1 Sep 2024
Cited by 1 | Viewed by 1366
Abstract
Secretogranin III (Scg3) is a diabetic retinopathy (DR)-restricted angiogenic factor identified in preclinical studies as a target for DR therapy. Previously, our group generated and characterized ML49.3, an anti-Scg3 monoclonal antibody (mAb) which we then converted into an EBP2 humanized antibody Fab fragment [...] Read more.
Secretogranin III (Scg3) is a diabetic retinopathy (DR)-restricted angiogenic factor identified in preclinical studies as a target for DR therapy. Previously, our group generated and characterized ML49.3, an anti-Scg3 monoclonal antibody (mAb) which we then converted into an EBP2 humanized antibody Fab fragment (hFab) with potential for clinical application. We also generated anti-Scg3 mT4 mAb and related EBP3 hFab. In this study, to identify the preferred hFab for DR therapy, we compared all four antibodies for binding, neutralizing and therapeutic activities in vitro and in vivo. Octet binding kinetics analyses revealed that ML49.3 mAb, EBP2 hFab, mT4 mAb and EBP3 hFab have Scg3-binding affinities of 35, 8.7, 0.859 and 0.116 nM, respectively. Both anti-Scg3 EBP2 and EBP3 hFabs significantly inhibited Scg3-induced proliferation and migration of human umbilical vein endothelial cells in vitro, and alleviated DR vascular leakage and choroidal neovascularization with high efficacy. Paired assays in DR mice revealed that intravitreally injected EBP3 hFab is 26.4% and 10.3% more effective than EBP2 hFab and aflibercept, respectively, for ameliorating DR leakage. In conclusion, this study confirms the markedly improved binding affinities of hFabs compared to mAbs and further identifies EBP3 hFab as the preferred antibody to develop for anti-Scg3 therapy. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Retinal Diseases)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-3
Back to TopTop