Ianors Iandiev

TL;DR: An overview of the neuroprotective and detrimental effects of Müller cell gliosis is provided, with accounts on the cellular signal transduction mechanisms and factors which are implicated in Müllercell-mediated neuroprotection, immunomodulation, regulation of Müllers cell proliferation, upregulation of intermediate filaments, glial scar formation, and the generation of neural progenitor/stem cells.

TL;DR: The present knowledge regarding the role of retinal glial cells in the uptake of glutamate, N-acetylaspartylglutamate, gamma-aminobutyric acid, glycine, and d-serine, as well as the degradation and removal of purinergic receptor agonists are summarized.

TL;DR: The data suggest that a disturbed fluid transport through Müller cells is (in addition to vascular leakage) a pathogenic factor contributing to the development of retinal edema.

TL;DR: A mechanism of postischemic glial cell swelling where a downregulation of their K(+) conductance prevents the emission of intracellularly accumulated K(+ ions, resulting in osmotically driven water fluxes from the blood into the glial cells via aquaporins is proposed.

TL;DR: The data show that glial cells in diabetic retinas are more sensitive to osmotic stress, which is associated with a decrease of K+ currents, than cells in control retinas, and is suggested that these alterations may be implicated in the development of diabetic retinal edema.