Increase in sICAM-1 and sVCAM-1 levels, as well as their correlation with high vitreous IL-6 and TNF-alpha concentrations in patients with PDR, seem to confirm the inflammatory-immune nature of this process. In diabetes, inadequate metabolic control remains an important risk factor in the development of PDR.

No abstract

Age-related macular degeneration (AMD) is a disease that causes varying degrees of blindness, which afflicts millions of adults in their later years. Preliminary changes occur during normal aging, but in some individuals the pathology leads to the development of AMD. The pathology seems to be a mixture of biochemical, cellular, and molecular events. Lipofuscinogenesis and early drusen genesis are in the early stages of AMD and their inhibition or reversal would dramatically increase the quality of vision in elderly people. The disease is characterized by abnormal extracellular deposits, known as drusen, which accumulate along the basal surface of the retinal pigmented epithelium RPE. Widespread drusen deposition is associated with retinal pigmented epithelial cell dysfunction and degeneration of the photoreceptors. Recent studies have shown that drusen contain a variety of immunomodulatory molecules, suggesting that the process of drusen formation involves local inflammatory events, including activation of the complement cascade. Molecular pathways involved in the etiology of this disease and the potential prospects of its treatment will be presented on the basis of the results of the current studies.

No abstract

Diabetic retinopathy constitutes the most frequent cause of vision loss in professionally active individuals. Progressive impairment of visual acuity results from massive fibrovascular proliferation involving the fundus of the eye, as well as from the apoptosis of the neuronal structures of the retina. The results of many clinical studies, both on experimental models and on human material, confirmed evident enhancement of this process in the course of diabetes. The programmed cell death of retinal ganglion cells predominantly occurs secondarily to caspase--dependent intracellular processes. This paper presents evidence for the considerable involvement of the caspase--dependent mechanism of apoptosis of retinal ganglion cells in the early stages of retinal changes associated with progressive impairment of visual acuity. The authors emphasize the necessity of comprehensive understanding of mechanisms that underlie the programmed death of neural cells in the eyes of patients with diabetes. This clinical problem becomes of vital importance in view of the constantly increasing incidence of diabetes and severe impairment associated with the disorders of carbohydrate metabolism. Identification of a key component involved in this process would enable attempts oriented at pharmacological blockade of apoptosis in the retinal ganglion cells of patients with diabetes (Adv Clin Exp Med 2015, 24, 3, 531-535).