Caspase-Dependent Apoptosis of Retinal Ganglion Cells During the Development of Diabetic Retinopathy

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 reti...

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Veröffentlicht in:Advances in clinical and experimental medicine : official organ Wroclaw Medical University 2015-05, Vol.24 (3), p.531-535
Hauptverfasser: Adamiec-Mroczek, Joanna, Zając-Pytrus, Hanna, Misiuk-Hojło, Marta
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Sprache:eng
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Zusammenfassung: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.
ISSN:1899-5276
DOI:10.17219/acem/31805