Relationship between VEGF expression and ganglion and photoreceptor cell densities in diabetic retinal layers

Abstract

INTRODUCTION: Hyperglycemia in diabetic retinopathy induces metabolic changes in the retina, which are triggered by oxidative stress and cause inflammation. Oxidative and inflammatory processes damage glial and neuron cells either indirectly or directly by inducing changes in the release and production of neurotrophic factors. The process of apoptosis and resultant decrease in ganglion density as a sign of cell degeneration occur in early diabetes mellitus. Recent research has found that early diabetic retinopathy involves the retinal neuron stimulating apoptosis in retinal ganglion and photoreceptor cells, along with increased vascular endothelial growth factor (VEGF), which causes retinal microvascular manifestations. This systematic review aimed to describe the relationship between VEGF expression and ganglion and photoreceptor densities in diabetic retinal layers.EVIDENCE ACQUISITION: The review searched research publications through reputable sources using the key words “vascular endothelial growth factor,” “diabetic retinopathy,” “neuroprotector,” and “neurodegeneration” to collect seven papers on the topic. The search was limited to experimental research articles, the subject areas of medicine and neuroscience, and available full-text reviews and articles.EVIDENCE SYNTHESIS: The initial phase of prolonged hyperglycemia damages retinal nerve cells. Neurodegenerative neurons play an important neuroprotective role by upregulating VEGF levels to prevent apoptosis. However, increasing VEGF over a long period triggers neovascularization, which leads to apoptosis and lowers retinal ganglion and photoreceptor cell densities.CONCLUSIONS: VEGFs act as an important liaison between retinal neuron death and retinal microvascular lesions.

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