Vascular and neuronal dysfunction are two common manifestations in ocular conditions, whereby inflammation is a pivotal process that is tightly linked to disease development and progression. Pathological neovascularization of the retina, the subretinal vasculature (choroid), the iris or the cornea is vision threatening in various ocular disorders across all age groups. Current therapies such as laser photocoagulation and anti-vascular endothelial growth factor (VEGF) therapy often show limited efficacy and possess adverse effects. Furthermore, recent evidence suggests that ocular metabolic dysfunction interacts with inflammatory responses and contribute to the progression of ocular disorders. However, our current knowledge on the intricate interplay between inflammation, aberrant metabolism, neovascularization and neural dysfunction remains limited. Neuronal dysfunction occurs early in vascular disease and may persist even after the vascular pathology is relieved. Most recent studies suggest that neuronal inflammatory and metabolic abnormalities primarily drive the vascular responses. Therefore, preserving neuronal integrity may prevent and treat vascular pathology.
Continuous efforts have been made to uncover the cellular responses to support neuronal survival in retinal degenerative diseases. Dry age-related macular degeneration and inherited retinal degenerative diseases, such as retinitis pigmentosa, are etiologically diverse group of blinding eye diseases. However, the cause of blinding at cellular level in great majority of these diseases is attributable to damage and death of retinal pigment epithelium (RPE) and/or photoreceptor (PR) cells. Inflammation is the most generalized pathological event in these diseases, but we still lack knowledge of how it could be effectively targeted to decrease RPE and PR cell death. Recent reports also revealed the primary role of disturbed metabolic balance between RPE and photoreceptor in PR degeneration. Further understanding of the mechanisms and how cells respond to compensate the alterations is needed. Glaucoma is an optic neuropathy that is often associated with a loss of retinal ganglion cells (RGCs) stereotypically as a result of increased intra-ocular pressure (IOP). Recently, emerging evidence has shown that aberrant metabolism of the RGCs may dispose the eye towards glaucoma, especially in the case of normotensive glaucoma (a type of glaucoma that is not due to an elevated IOP). Microglial response is thought to play an essential role in RGCs health, whereby overactivation is detrimental. Therefore, comprehensive investigations on the interaction between IOP, RGC metabolism and microglial activity during the development of glaucoma are necessary. A thorough understanding on this relationship would allow to design better pharmaceutical or surgical interventions for this prevalent disease.
The aim of this Research Topic is to understand the neuronal metabolic and inflammatory responses, as well as retinal cell-cell interactions (such as neuron-RPE, neuron-glia, neuron-endothelium) in retinal degenerative disorders.
We welcome submissions focusing on new evidence in ocular disease development and progression, as well as the exploration of disease treatment from the inflammatory and metabolic aspects. Original Research articles, reviews, mini-reviews and case reports will be preferred. We welcome manuscripts addressing, but not restricted to, the following:
• Investigation of the role of inflammatory responses linked to neurodegeneration in retinal cells;
• Investigation of the role of metabolic regulation in retinal cells, in both physiological and pathological processes;
• Assessment of the efficacy and safety of current treatments;
• Exploration of potential new therapeutic targets.
Vascular and neuronal dysfunction are two common manifestations in ocular conditions, whereby inflammation is a pivotal process that is tightly linked to disease development and progression. Pathological neovascularization of the retina, the subretinal vasculature (choroid), the iris or the cornea is vision threatening in various ocular disorders across all age groups. Current therapies such as laser photocoagulation and anti-vascular endothelial growth factor (VEGF) therapy often show limited efficacy and possess adverse effects. Furthermore, recent evidence suggests that ocular metabolic dysfunction interacts with inflammatory responses and contribute to the progression of ocular disorders. However, our current knowledge on the intricate interplay between inflammation, aberrant metabolism, neovascularization and neural dysfunction remains limited. Neuronal dysfunction occurs early in vascular disease and may persist even after the vascular pathology is relieved. Most recent studies suggest that neuronal inflammatory and metabolic abnormalities primarily drive the vascular responses. Therefore, preserving neuronal integrity may prevent and treat vascular pathology.
Continuous efforts have been made to uncover the cellular responses to support neuronal survival in retinal degenerative diseases. Dry age-related macular degeneration and inherited retinal degenerative diseases, such as retinitis pigmentosa, are etiologically diverse group of blinding eye diseases. However, the cause of blinding at cellular level in great majority of these diseases is attributable to damage and death of retinal pigment epithelium (RPE) and/or photoreceptor (PR) cells. Inflammation is the most generalized pathological event in these diseases, but we still lack knowledge of how it could be effectively targeted to decrease RPE and PR cell death. Recent reports also revealed the primary role of disturbed metabolic balance between RPE and photoreceptor in PR degeneration. Further understanding of the mechanisms and how cells respond to compensate the alterations is needed. Glaucoma is an optic neuropathy that is often associated with a loss of retinal ganglion cells (RGCs) stereotypically as a result of increased intra-ocular pressure (IOP). Recently, emerging evidence has shown that aberrant metabolism of the RGCs may dispose the eye towards glaucoma, especially in the case of normotensive glaucoma (a type of glaucoma that is not due to an elevated IOP). Microglial response is thought to play an essential role in RGCs health, whereby overactivation is detrimental. Therefore, comprehensive investigations on the interaction between IOP, RGC metabolism and microglial activity during the development of glaucoma are necessary. A thorough understanding on this relationship would allow to design better pharmaceutical or surgical interventions for this prevalent disease.
The aim of this Research Topic is to understand the neuronal metabolic and inflammatory responses, as well as retinal cell-cell interactions (such as neuron-RPE, neuron-glia, neuron-endothelium) in retinal degenerative disorders.
We welcome submissions focusing on new evidence in ocular disease development and progression, as well as the exploration of disease treatment from the inflammatory and metabolic aspects. Original Research articles, reviews, mini-reviews and case reports will be preferred. We welcome manuscripts addressing, but not restricted to, the following:
• Investigation of the role of inflammatory responses linked to neurodegeneration in retinal cells;
• Investigation of the role of metabolic regulation in retinal cells, in both physiological and pathological processes;
• Assessment of the efficacy and safety of current treatments;
• Exploration of potential new therapeutic targets.
