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- W51564645 abstract "The key to identifying the type of diabetic maculopathy is determining the status of posterior vitreous adhesion. In the pathological state, the breakdown of the internal and external blood-retina barrier is evident, however the mechanism is usually complex. The common denominator for these disorders are Muller glial cells, which mediate in maintaining the blood-retina barrier by linking the vessels, neurons and the vitreous in anatomical network and into functional dependence. The breakdown of the blood-retina barrier results in proliferation of Muller cells. Molecular changes in these cells increase endothelial barrier properties, but also induce pathological processes on the vitreo-retinal junction, resulting in increased adhesiveness of the collagen fibers of vitreous to retinal internal limiting membrane. The ability of Muller cells to reactive gliosis is influenced by the healthy functioning of the retinal pigment epithelium, which is a source of trophic factors necessary for appropriate Muller cells morphogenesis. Vitrectomy with the removal of ILM eliminates the vitreofoveal interface pathology, additionally provoking reactive gliosis within the macula. Intraoperative use of anti-VEGF supports short-term tightness of the blood-retina barrier in the perioperative neuralgic period. In the future, supplying astrocytes may be a strategy that will allow not only the inhibition of pathological neovascularization but also the restoration of the physiological network of capillaries in avascular retina areas. The delivery of recombinant PEDF allows for the recovery of Muller cells, and thus creates the conditions favourable for the survival of nerve cells in loss of retinal homeostasis." @default.
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- W51564645 date "2010-01-01" @default.
- W51564645 modified "2023-09-29" @default.
- W51564645 title "Müller glial cells--the mediators of vascular disorders with vitreomacular interface pathology in diabetic maculopathy." @default.
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