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

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

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