Патогенез діабетичного макулярного набряку: роль гліального компонента (огляд літератури та власні дані). (Ukrainian)

Pathogenesis of diabetic macular edema: role of the glial factor (literature review and own data). (English)

The review presents modern data on the pathogenesis of diabetic macular edema. Today, a new understanding of the pathophysiology of diabetic retinal lesions includes structural dysfunction of the neurovascular unit (NVU) of the retina. NVU includes astrocytes and Müller cells, it is a physical and biochemical link between neurons, glia, vascular network in situ, acts as an interface between neurons and the vascular system, and is a key regulator of neuronal metabolism. The close interdependence of glial cells, pericytes and neurons contributes to the formation of a barrier between the blood and the retina, which controls the flow of fluid and hemotransmissive metabolites into the glial parenchyma of eye tissue. Glial components of NVU contribute to the survival of neuronal ganglion cells and photoreceptors, stabilization of the retinal structure, and modulation of inflammatory and immune reactions. It has been shown that intercellular interactions between blood vessels and neurons play a critical role in the formation of blood-retinal barrier whose activity is modulated by the state of retinal endothelial communications. In diabetes, the blood-retinal barrier breaks down already at the early stage of diabetic retinopathy, changing the structure and function of most types of cells in the retina; however, the molecular mechanisms of this pathological process in diabetes are not sufficiently studied and require the search for new therapeutic strategies, in particular, with the participation of clusterin. Emphasis is placed on the significance of dysfunction in the neurovascular unit of the retina for the development of complications in diabetes. Increased attention is paid to microglial activation, Müller cell dysfunction, damage to the blood-retinal barrier, as well as the role of clusterin and fractalkine in barrier cytoprotection. [ABSTRACT FROM AUTHOR]

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