Special Issue "Diabetic Retinopathy"

Special Issue Editor

Prof. Dr. Winfried M. Amoaku
E-Mail Website
Guest Editor
Division of Ophthalmology and Visual Sciences, B Floor, Eye and ENT Building, Queen’s Medical Centre, University of Nottingham, Nottingham NG7 2UH, UK
Interests: disease burden; pathogenesis/treatments for AMD; other retinal diseases (clinical and laboratory)

Special Issue Information

Dear Colleagues,

Diabetic retinopathy (DR) is a common cause of visual loss across the world, especially in the working-age group. As the prevalence of diabetes mellitus (DM) continues to increase worldwide, the occurrence of DR and diabetic macular oedema (DMO) continues to climb. The risks for DR and DR are known, and our understanding of the underlying pathophysiology has advanced recently. The introduction of pharmacologic therapies, and modern diagnostic modalities of optical coherence tomography (OCT) and more recently, OCT angiography (OCT-A) has resulted in better management and outcomes for DR, with vision preservation in some patients. However, early detection of DR remains crucial in achieving early treatment and better visual outcomes.

This Special Issue aims to provide updated information, including reviews, original clinical and laboratory studies, population studies, development of new tools, disease detection, and service delivery in DR and diabetic care from across the different continents.

Prof. Dr. Winfried Amoaku
Guest Editor

Manuscript Submission Information

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Keywords

  • Diabetes
  • Diabetic retinopathy (DR)
  • Diabetic macular oedema
  • DR understanding
  • DR clinical management
  • DR screening/detection
  • DR service delivery
  • DR visual impairment

Published Papers (3 papers)

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Research

Article
Diabetic Retinopathy Screening Programme: Attendance, Barriers and Enablers amongst Young People with Diabetes Mellitus Aged 12–26 Years
Int. J. Transl. Med. 2021, 1(3), 154-162; https://0-doi-org.brum.beds.ac.uk/10.3390/ijtm1030011 - 22 Sep 2021
Viewed by 189
Abstract
The study aim is to investigate characteristics, barriers and enablers for attendance at the Diabetic Eye Screening Programme Northern Ireland (DESPNI) among people with diabetes aged 12–26 years. A mixed-methods approach with retrospective analysis and prospective, questionnaire-based data collection was completed. Data were [...] Read more.
The study aim is to investigate characteristics, barriers and enablers for attendance at the Diabetic Eye Screening Programme Northern Ireland (DESPNI) among people with diabetes aged 12–26 years. A mixed-methods approach with retrospective analysis and prospective, questionnaire-based data collection was completed. Data were analysed using ordinal logistic regression. A questionnaire collected information on barriers and enablers to attending DESPNI. Age, diabetes duration, attendance at diabetes clinic and lower HbA1c values were significantly associated with better attendance. Those aged 12–15 were more likely to attend screening than 16–26 years, odds ratio (OR) 4.01. Subjects diagnosed less than 5 years were more likely to attend than those with longer diabetes duration (OR = 2.52, p =< 0.001). Subjects who attended diabetes clinics were more likely to attend screening (OR = 1.89, p =< 0.001) and have a lower HbA1c (OR = 1.46, p =< 0.001). Questionnaires revealed major barriers to attendance which included inconvenient appointment times, lack of access and poor communication. While many subjects were aware of the impact of diabetes on the eye, many had little understanding of screening. This study provides pivotal information on potential barriers and enablers for young people attending eye screening. We suggest modest changes such as convenient appointment times, clearer communication and one-stop clinics could improve attendance. Full article
(This article belongs to the Special Issue Diabetic Retinopathy)
Article
Interleukin-6 Trans-Signaling Mediated Regulation of Paracellular Permeability in Human Retinal Endothelial Cells
Int. J. Transl. Med. 2021, 1(2), 137-153; https://0-doi-org.brum.beds.ac.uk/10.3390/ijtm1020010 - 16 Sep 2021
Viewed by 270
Abstract
Long-term hyperglycemia-mediated oxidative stress and inflammation lead to the blood-retinal barrier (BRB) dysfunction and increased vascular permeability associated with diabetic retinopathy (DR). Interleukin-6 (IL-6) is one of the primary mediators of retinal vascular inflammation. IL-6 signaling through its membrane-bound IL-6 receptor is known [...] Read more.
Long-term hyperglycemia-mediated oxidative stress and inflammation lead to the blood-retinal barrier (BRB) dysfunction and increased vascular permeability associated with diabetic retinopathy (DR). Interleukin-6 (IL-6) is one of the primary mediators of retinal vascular inflammation. IL-6 signaling through its membrane-bound IL-6 receptor is known as classical signaling, and through a soluble IL-6 receptor (sIL-6R) is known as trans-signaling. Increasing evidence suggests that classical signaling is primarily anti-inflammatory, whereas trans-signaling induces the pro-inflammatory effects of IL-6. The purpose of this study was to compare the effects of these two pathways on paracellular permeability and expression of genes involved in inter-endothelial junctions in human retinal endothelial cells (HRECs). IL-6 trans-signaling activation caused significant disruption to paracellular integrity, with increased paracellular permeability, and was associated with significant changes in gene expression related to adherens, tight, and gap junctions. IL-6 classical signaling did not alter paracellular resistance in HRECs and had no distinct effects on gene expression. In conclusion, IL-6 trans-signaling, but not classical signaling, is a major mediator of the increased paracellular permeability characteristic of inner BRB breakdown in diabetic retinopathy. This study also identified potential inter-endothelial junction genes involved in the IL-6 trans-signaling mediated regulation of paracellular permeability in HRECs. Full article
(This article belongs to the Special Issue Diabetic Retinopathy)
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Article
Toll-Like Receptor Signalling Pathways Regulate Hypoxic Stress Induced Fibroblast Growth Factor but Not Vascular Endothelial Growth Factor-A in Human Microvascular Endothelial Cells
Int. J. Transl. Med. 2021, 1(1), 25-38; https://0-doi-org.brum.beds.ac.uk/10.3390/ijtm1010003 - 27 May 2021
Viewed by 755
Abstract
Retinal diseases are the leading causes of irreversible blindness worldwide. The role of toll-like receptor (TLR) signalling mechanisms (MyD88 and TRIF) in the production of pro-angiogenic growth factors from human microvascular endothelial cells (HMEC-1) under hypoxic stress remains unexplored. HMEC-1 was incubated under [...] Read more.
Retinal diseases are the leading causes of irreversible blindness worldwide. The role of toll-like receptor (TLR) signalling mechanisms (MyD88 and TRIF) in the production of pro-angiogenic growth factors from human microvascular endothelial cells (HMEC-1) under hypoxic stress remains unexplored. HMEC-1 was incubated under normoxic (5% CO2 at 37 °C) and hypoxic (1% O2, 5% CO2, and 94% N2; at 37 °C) conditions for 2, 6, 24, and 48 h, respectively. For TLR pathway analysis, HMEC-1 was pre-treated with pharmacological inhibitors (Pepinh-MyD88 and Pepinh-TRIF) and subjected to normoxia and hypoxia conditions. Gene and protein expressions of vascular endothelial growth factor-A (VEGF-A), fibroblast growth factor (FGF-2), hypoxia inducible factor 1-alpha (HIF1-α) were performed using quantitative polymerase chain reaction (qPCR), ELISA, and Western blot methodologies. Levels of TLR3 and TLR4 were analysed by flow cytometry. Under hypoxia, levels of VEGF-A and FGF-2 were elevated in a time-dependent fashion. Inhibition of MyD88 and TRIF signalling pathways decreased FGF-2 levels but failed to modulate the secretion of VEGF-A from HMEC-1. Blocking a known regulator, endothelin receptor (ETR), also had no effect on VEGF-A secretion from HMEC-1. Overall, this study provides the proof-of-concept to target TLR signalling pathways for the management of blinding retinal diseases. Full article
(This article belongs to the Special Issue Diabetic Retinopathy)
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