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Molecular Advances in Pathogenesis and Treatment of Diabetic Retinopathy
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Molecular Advances in Pathogenesis and Treatment of Diabetic Retinopathy

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: 20 June 2024 | Viewed by 4298

Special Issue Editor

Prof. Dr. Rafael Simó

E-Mail Website
Guest Editor
1. Vall d'Hebron Research Institute (VHIR), Hospital Universitari Vall d'Hebron, 08035 Barcelona, Spain
2. CIBER de Diabetes i Enfermedades Metabólicas Asociadas (ISCIII), 28220 Madrid, Spain
3. Derpartment of Medicine-Endocrinology, Autonomous Univeristy of Barcelona, 08035 Bacelona, Spain
Interests: diabetes mellitus; complications of diabetes; diabetes microangiopathy; diabetic retinopathy; neurodegeneration; clinical diabetes; personalized treatment of diabetes
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

As you know, the concept of diabetic retinopathy (DR) as a microvascular disease has evolved, and rather than being a merely microvascular disease, it is now considered a more complex diabetic complication in which neurodegeneration plays a significant role. Glial activation, neurodegeneration, and neurovascular unit (NVU) impairment are primary events in the pathogenesis of DR and have been observed to occur before overt microangiopathy in experimental models of DR and in the retina of diabetic donors. Therefore, better knowledge of the underlying mechanism involved in NVU impairment will be important in the design of new therapeutic approaches for early stages of DR. 

In advanced stages of DR, more aggressive treatments such laser treatment, intravitreal injections of anti-VEGF agents, or corticosteroids are needed. However, these treatments are expensive and are associated with significant side effects. In addition, although anti-VEGFs are the first line treatment, around 50% of patients are nonresponders in the long term. Therefore, a more personalized treatment based on a better phenotyping of the disease is needed. 

In this Special Issue, original articles, reviews, and full reviews on new insights in the pathogenesis or treatment of early or advanced stages of DR are welcome. 

Prof. Dr. Rafael Simó
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

  • diabetic retinopathy
  • pathophysiology of diabetic retinopathy
  • molecular mediators of diabetic retinopathy
  • retinal neurodegeneration
  • new treatments for diabetic retinopathy
  • personalized therapy

Published Papers (3 papers)

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Research

13 pages, 1524 KiB  
Article
Release of Pro-Inflammatory/Angiogenic Factors by Retinal Microvascular Cells Is Mediated by Extracellular Vesicles Derived from M1-Activated Microglia
by Elena Beltramo, Aurora Mazzeo and Massimo Porta
Int. J. Mol. Sci. 2024, 25(1), 15; https://doi.org/10.3390/ijms25010015 - 19 Dec 2023
Viewed by 1315
Abstract
The interactions between the neuronal and vascular sides of the retina during diabetic retinopathy (DR) have gained increasing attention. Microglia is responsible for the immune response to inflammation inside the retina, which could be mediated by paracrine signals carried by extracellular vesicles (EVs). [...] Read more.
The interactions between the neuronal and vascular sides of the retina during diabetic retinopathy (DR) have gained increasing attention. Microglia is responsible for the immune response to inflammation inside the retina, which could be mediated by paracrine signals carried by extracellular vesicles (EVs). We aimed to characterize EVs released from immortalized human microglial cells in inflammation and investigate their effects on the retinal microvasculature and the anti-inflammatory potential of thiamine in this context. M1 pro-inflammatory polarization in microglia was induced through a cytokine cocktail. EVs were isolated from the supernatants, characterized, and used to stimulate human retinal endothelial cells (HRECs) and pericytes (HRPs). Microvascular cell functions and their release of pro-inflammatory/angiogenic factors were assessed. M1-derived EVs showed increased content of miR-21, miR-155, CCL2, MMP2, and MMP9, and enhanced apoptosis, proliferation, migration, and ROS production in HRPs and HRECs. IL-1β, IL-6, MMP9, CCL2, and VEGF release increased in HRPs exposed to M1-derived EVs, while HRECs showed augmented IL-6, Ang2, VEGF, and PDFG-B. Addition of thiamine to M1-microglial cultures reverted most of these effects. In conclusion, M1-derived EVs stimulate functional changes and secretion of pro-inflammatory/angiogenic molecules in microvascular cells, exacerbating inflammatory damage and retinopathy features. Thiamine added to microglia exerts anti-inflammatory effects. Full article
(This article belongs to the Special Issue Molecular Advances in Pathogenesis and Treatment of Diabetic Retinopathy)
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11 pages, 4200 KiB  
Article
Progressive Thinning of Retinal Nerve Fiber Layer/Ganglion Cell Layer (RNFL/GCL) as Biomarker and Pharmacological Target of Diabetic Retinopathy
by Gianpaolo Zerbini, Silvia Maestroni, Ilaria Viganò, Andrea Mosca, Renata Paleari, Daniela Gabellini, Silvia Galbiati and Paolo Rama
Int. J. Mol. Sci. 2023, 24(16), 12672; https://doi.org/10.3390/ijms241612672 - 11 Aug 2023
Cited by 1 | Viewed by 916
Abstract
Diabetes-driven retinal neurodegeneration has recently been shown to be involved in the initial phases of diabetic retinopathy, raising the possibility of setting up a preventive strategy based on early retinal neuroprotection. To make this possible, it is crucial to identify a biomarker for [...] Read more.
Diabetes-driven retinal neurodegeneration has recently been shown to be involved in the initial phases of diabetic retinopathy, raising the possibility of setting up a preventive strategy based on early retinal neuroprotection. To make this possible, it is crucial to identify a biomarker for early retinal neurodegeneration. To this end, in this study, we verified and confirmed that, in the Akita mouse model of diabetes, the thinning of the retinal nerve fiber layer/ganglion cell layer (the RNFL/GCL—the layer that contains the retinal ganglion cells) precedes the death of these same cells, suggesting that this dysfunction is a possible biomarker of retinal neurodegeneration. We then confirmed the validity of this assumption by starting a neuroprotective treatment (based on nerve growth factor eye drops) in concert with the first demonstration of RNFL/GCL thinning. In this way, it was possible not only to avoid the loss of retinal ganglion cells but also to prevent the subsequent development of the microvascular stage of diabetic retinopathy. In conclusion, in the case of diabetes, the thinning of the RNFL/GCL appears to be both a valid biomarker and a pharmacological target of diabetic retinopathy; it precedes the development of vascular dysfunctions and represents the ideal starting point for prevention. Full article
(This article belongs to the Special Issue Molecular Advances in Pathogenesis and Treatment of Diabetic Retinopathy)
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19 pages, 4060 KiB  
Article
Untargeted Multiomics Approach Coupling Lipidomics and Metabolomics Profiling Reveals New Insights in Diabetic Retinopathy
by Patricia Ancel, Jean Charles Martin, Elisa Doukbi, Marie Houssays, Pierre Gascon, Maud Righini, Frédéric Matonti, Ljubica Svilar, Marie Valmori, Catherine Tardivel, Nicolas Venteclef, Jean Baptiste Julla, Jean François Gautier, Noémie Resseguier, Anne Dutour and Bénédicte Gaborit
Int. J. Mol. Sci. 2023, 24(15), 12053; https://doi.org/10.3390/ijms241512053 - 27 Jul 2023
Cited by 3 | Viewed by 1642
Abstract
Diabetic retinopathy (DR) is a microvascular complication of diabetes mellitus (DM) which is the main cause of vision loss in the working-age population. Currently known risk factors such as age, disease duration, and hemoglobin A1c lack sufficient efficiency to distinguish patients with early [...] Read more.
Diabetic retinopathy (DR) is a microvascular complication of diabetes mellitus (DM) which is the main cause of vision loss in the working-age population. Currently known risk factors such as age, disease duration, and hemoglobin A1c lack sufficient efficiency to distinguish patients with early stages of DR. A total of 194 plasma samples were collected from patients with type 2 DM and DR (moderate to proliferative (PDR) or control (no or mild DR) matched for age, gender, diabetes duration, HbA1c, and hypertension. Untargeted lipidomic and metabolomic approaches were performed. Partial-least square methods were used to analyze the datasets. Levels of 69 metabolites and 85 lipid species were found to be significantly different in the plasma of DR patients versus controls. Metabolite set enrichment analysis indicated that pathways such as metabolism of branched-chain amino acids (methylglutaryl carnitine p = 0.004), the kynurenine pathway (tryptophan p < 0.001), and microbiota metabolism (p-Cresol sulfate p = 0.004) were among the most enriched deregulated pathways in the DR group. Moreover, Glucose-6-phosphate (p = 0.001) and N-methyl-glutamate (p < 0.001) were upregulated in DR. Subgroup analyses identified a specific signature associated with PDR, macular oedema, and DR associated with chronic kidney disease. Phosphatidylcholines (PCs) were dysregulated, with an increase of alkyl-PCs (PC O-42:5 p < 0.001) in DR, while non-ether PCs (PC 14:0–16:1, p < 0.001; PC 18:2–14:0, p < 0.001) were decreased in the DR group. Through an unbiased multiomics approach, we identified metabolites and lipid species that interestingly discriminate patients with or without DR. These features could be a research basis to identify new potential plasma biomarkers to promote 3P medicine. Full article
(This article belongs to the Special Issue Molecular Advances in Pathogenesis and Treatment of Diabetic Retinopathy)
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