Role of the Redox System in Initiation of a Regenerative Response of Neural Eye Tissues in Vertebrates

The review examines the role of oxidative stress (OS) in the primary response of the neural eye tissue cells to damage and degenerative processes. The imbalance (homeostasis) of the redox system towards oxidative processes underlies the development of OS. OS can be used as a part of the protective mechanism initiating the processes of healing and regeneration of damaged tissues. Violation of redox homeostasis and OS development triggers an inflammatory response and immune response in the retina. The main reactions to stress (release of ATP, calcium ions, and reactive oxygen species (ROS) into the extracellular space, attraction of exogenous immune cells, activation of endogenous macro- and microglia, apoptosis of neurons) are universal and conservative in all vertebrates. However, with the similarity of some parts of cellular and molecular processes, there are evolutionary fixed functional differences in the regenerative response of retinal cells, and the final result in different vertebrate species is not equivalent. This determines the choice of regeneration strategies: activation of endogenous stem/progenitor cells and/or reprogramming of differentiated cells (retinal pigment epithelium, Muller glia). The detection of key signaling pathways, through which the effect of OS on regenerative responses is realized after damage and pathology of the neural tissues of the vertebral eye, will contribute to the choice of optimal strategies of the cell and/or gene therapy to activate the endogenic regenerative potential of retinal neural tissue in humans.