The role of gap junctions in cell death and neuromodulation in the retina
Gergely Szarka1
Márton Balogh1
Ádám J.Tengölics1
Alma Ganczer1
Béla Völgyi2
Tamás Kovács-Öller3
1.János Szentágothai Research Centre,University of Pécs,Pécs,Hungary;Retinal Electrical Synapses Research Group,National Brain Research Program (NAP 2.0),Hungarian Academy of Sciences,Budapest,Hungary;Department of Experimental Zoology and Neurobiology,University of Pécs,Pécs,Hungary2.János Szentágothai Research Centre,University of Pécs,Pécs,Hungary;Retinal Electrical Synapses Research Group,National Brain Research Program (NAP 2.0),Hungarian Academy of Sciences,Budapest,Hungary;Department of Experimental Zoology and Neurobiology,University of Pécs,Pécs,Hungary;Medical School,University of Pécs,Pécs,Hungary3.János Szentágothai Research Centre,University of Pécs,Pécs,Hungary;Retinal Electrical Synapses Research Group,National Brain Research Program (NAP 2.0),Hungarian Academy of Sciences,Budapest,Hungary;Medical School,University of Pécs,Pécs,Hungary
摘要：Vision altering diseases, such as glaucoma, diabetic retinopathy, age-related macular degeneration, myopia, retinal vascular disease, traumatic brain injuries and others cripple many lives and are projected to continue to cause anguish in the foreseeable future. Gap junctions serve as an emerging target for neuromodulation and possible regeneration as they directly connect healthy and/or diseased cells, thereby playing a crucial role in pathophysiology. Since they are permeable for macromolecules, able to cross the cellular barriers, they show duality in illness as a cause and as a therapeutic target. In this review, we take recent advancements in gap junction neuromodulation (pharmacological blockade, gene therapy, electrical and light stimulation) into account, to show the gap junction's role in neuronal cell death and the possible routes of rescuing neuronal and glial cells in the retina succeeding illness or injury.
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论文发表日期：2021-10-28
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：10( 1911-1920 )
英文信息