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Cells
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Cellular and Molecular Mechanisms of Neurodegeneration and Vascular Damage in...
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Cellular and Molecular Mechanisms of Neurodegeneration and Vascular Damage in Diabetic Retinopathy

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Nervous System".

Deadline for manuscript submissions: closed (31 July 2022) | Viewed by 5491

Special Issue Editor

Prof. Dr. Giovanni Casini

E-Mail Website
Guest Editor
Department of Biology, University of Pisa, Pisa, Italy
Interests: neuroprotection; physiology and pathology of the retina; physiology and pathology of the neurovascular unit; regulation of growth factor expression; nutraceuticals
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Diabetic retinopathy (DR) is a common complication of diabetes that constitutes a major cause of vision impairment worldwide. It is a multifactorial progressive disease characterized by an extremely complex pathogenesis involving different factors and a variety of pathophysiologic mechanisms causing the dysregulation of a number of mediators, including growth factors, neurotrophic factors, cytokines/chemokines, vasoactive agents, and inflammatory and adhesion molecules. Classically, DR has been considered as a microvascular disease, but in recent years, the contribution of neuroretinal degeneration has been recognized. In fact, neuronal, glial, and vascular cells are known to be intimately connected in the neurovascular unit, and recent evidence indicates that dysfunctions of this unit play a central role in the development of DR. In particular, since neurons are the most fragile and demanding cellular elements in the retina, it is conceivable that they are the first to be affected by the drastic changes in the retinal microenvironment caused by high glucose. In summary, it appears that both retinal neurons and vessels are affected in DR; therefore, the question is what kind of relationship, if any, exists between neuronal and vascular damage in DR and what role, if any, is played by the glial elements of the retina. Although vascular endothelial growth factor (VEGF) has been identified as the main driver of the vascular alterations and a role of VEGF has also been recognized in neuronal survival, a comprehensive knowledge of the mediators that are involved in the crosslink between neurodegeneration and vascular changes is still lacking.

This Special Issue welcomes contributions that may help in clarifying the involvement of the different cellular components of the retina (neurons, glial cells, and endothelial cells) in DR and the relationships between them in the progression of the disease. In this context, any evidence of treatments that may act on these mechanisms and reduce the impact of the disease will also be appreciated.

Articles will be peer-reviewed and published in the open access journal Cells. I look forward to your contributions. 

Sincerely,

Prof. Giovanni Casini
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. Cells is an international peer-reviewed open access semimonthly 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

  • Neuroprotection
  • Vascular endothelial growth factor
  • Neurovascular unit
  • Müller cells
  • Blood–retina barrier
  • Oxidative stress
  • Inflammation
  • Cell death

Published Papers (2 papers)

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Research

18 pages, 5968 KiB  
Article
A Promising Combination: PACAP and PARP Inhibitor Have Therapeutic Potential in Models of Diabetic and Hypertensive Retinopathies
by Etelka Pöstyéni, Krisztina Szabadfi, György Sétáló, Jr. and Robert Gabriel
Cells 2021, 10(12), 3470; https://doi.org/10.3390/cells10123470 - 9 Dec 2021
Cited by 5 | Viewed by 2430
Abstract
Diabetes and hypertension are complex pathologies with increasing prevalence nowadays. Their interconnected pathways are frequently manifested in retinopathies. Severe retinal consequences and their tight connections as well as their possible treatments are particularly important to retinal research. In the present, work we induced [...] Read more.
Diabetes and hypertension are complex pathologies with increasing prevalence nowadays. Their interconnected pathways are frequently manifested in retinopathies. Severe retinal consequences and their tight connections as well as their possible treatments are particularly important to retinal research. In the present, work we induced diabetes with streptozotocin in spontaneously hypertensive rats and treated them either with PACAP or olaparib and alternatively with both agents. Morphological and immunohistochemical analyses were carried out to describe cell-specific changes during pathologies and after different treatments. Diabetes and hypertension caused massive structural and cellular changes especially when they were elicited together. Hypertension was crucial in the formation of ONL and OPL damage while diabetes caused significant differences in retinal thickness, OPL thickness and in the cell number of the GCL. In diabetes, double neuroprotective treatment ameliorated changes of calbindin-positive cells, rod bipolar cells and dopaminergic amacrine cells. Double treatment was curative in hypertensive diabetic rat retinas, especially in the case of rod bipolar and parvalbumin-positive cells compared to untreated or single-treated retinas. Our results highlighted the promising therapeutic benefits of olaparib and PACAP in these severe metabolic retinal disorders. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Neurodegeneration and Vascular Damage in Diabetic Retinopathy)
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15 pages, 2576 KiB  
Article
Does Hyperglycemia Cause Oxidative Stress in the Diabetic Rat Retina?
by Mohammad Shamsul Ola
Cells 2021, 10(4), 794; https://doi.org/10.3390/cells10040794 - 2 Apr 2021
Cited by 14 | Viewed by 2361
Abstract
Diabetes, being a metabolic disease dysregulates a large number of metabolites and factors. However, among those altered metabolites, hyperglycemia is considered as the major factor to cause an increase in oxidative stress that initiates the pathophysiology of retinal damage leading to diabetic retinopathy. [...] Read more.
Diabetes, being a metabolic disease dysregulates a large number of metabolites and factors. However, among those altered metabolites, hyperglycemia is considered as the major factor to cause an increase in oxidative stress that initiates the pathophysiology of retinal damage leading to diabetic retinopathy. Diabetes-induced oxidative stress in the diabetic retina and its damaging effects are well known, but still, the exact source and the mechanism of hyperglycemia-induced reactive oxygen species (ROS) generation especially through mitochondria remains uncertain. In this study, we analyzed precisely the generation of ROS and the antioxidant capacity of enzymes in a real-time situation under ex vivo and in vivo conditions in the control and streptozotocin-induced diabetic rat retinas. We also measured the rate of flux through the citric acid cycle by determining the oxidation of glucose to CO2 and glutamate, under ex vivo conditions in the control and diabetic retinas. Measurements of H2O2 clearance from the ex vivo control and diabetic retinas indicated that activities of mitochondrial antioxidant enzymes are intact in the diabetic retina. Short-term hyperglycemia seems to influence a decrease in ROS generation in the diabetic retina compared to controls, which is also correlated with a decreased oxidation rate of glucose in the diabetic retina. However, an increase in the formation of ROS was observed in the diabetic retinas compared to controls under in vivo conditions. Thus, our results suggest of diabetes/hyperglycemia-induced non-mitochondrial sources may serve as major sources of ROS generation in the diabetic retina as opposed to widely believed hyperglycemia-induced mitochondrial sources of excess ROS. Therefore, hyperglycemia per se may not cause an increase in oxidative stress, especially through mitochondria to damage the retina as in the case of diabetic retinopathy. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Neurodegeneration and Vascular Damage in Diabetic Retinopathy)
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