Abstract
The retina is composed of neural networks that are responsible for visual function, and vascular networks that support the tissue. Although vascular targeting therapies for retinal diseases have recently been developed, therapies directly targeting the neuronal component of these diseases have yet to be developed. Here, we review recent studies describing the pathological signaling that occurs within the neuronal cells of retinal disease models. The molecular changes caused by endogenous or exogenous factors in the retinal neural cells and the molecular events involved in neuroinflammation are illustrated. These underlying molecular mechanisms reveal promising targets for new therapeutic approaches for retinal neural disorders.
Highlights
The retina is composed of neural networks that are responsible for visual function, and vascular networks that support the tissue
Data of leukostasis in the retinal vessels and vascular leakage assessed by measuring the retinal albumin, as well as molecular expression of inflammatory molecules such as TNF-α, ICAM-1, and NF-κB in the retina, are all suppressed in the diabetic model mice derived from the vascular endothelial growth factor (VEGF) conditional knockout mice generated using Cre-loxP system, in which Cre-recombinase is selectively expressed in the Müller glial cells
Studies in mice with a retina-specific knockout of suppressor of cytokine signaling 3 (SOCS3), a negative feedback intracellular molecule of STAT3, showed that activated STAT3 is elevated in the EIU model; this activated STAT3 accelerates the posttranscriptional decrease in rhodopsin, a visual pigment expressed in the rod photoreceptor cells
Summary
The retina is composed of neural networks that are responsible for visual function, and vascular networks that support the tissue. Results of these studies have indicated that oxidative stress [6,7,8] and inflammatory signaling [7,8,9,10,11] in the retinal neural tissue are deeply involved in the disease-related mechanisms. The increased accumulation of ROS in the diabetic retina probably results from both an increase in ROS generation, at least in part due to high glucose level, and a decrease in the expression of anti-oxidative enzymes as previously shown in the animal model [6], even when there is no genetic defect.
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