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Front. Neurosci. | doi: 10.3389/fnins.2018.00834

The role of endogenous neuroprotective mechanisms in the prevention of retinal ganglion cells degeneration

  • 1Department of Physiology, Medical University of Silesia, Poland
  • 2Dipartimento di Scienze del Farmaco, Università degli Studi di Pavia, Italy

Retinal neurons are not able to undergo spontaneous regeneration in response to damage. A variety of stressors, i.e., UV radiation, high temperature, ischemia, allergens, and others, induce reactive oxygen species production, resulting in consecutive alteration of stress-response gene expression and finally can lead to cell apoptosis. Neurons have developed their own endogenous cellular protective systems. Some of them are preventing cell death and others are allowing functional recovery after injury. The high efficiency of these mechanisms is crucial for cell survival. In this review we focus on the contribution of the most recently studied endogenous neuroprotective factors involved in retinal ganglion cell (RGC) survival, among which, neurotrophic factors and their signaling pathways, processes regulating the redox status, and different pathways regulating cell death are the most important. Additionally, we summarize currently ongoing clinical trials for therapies for RGC degeneration and optic neuropathies, including glaucoma. Knowledge of the endogenous cellular protective mechanisms may help in the development of effective therapies and potential novel therapeutic targets in order to achieve progress in the treatment of retinal and optic nerve diseases.

Keywords: retinal ganglion cell, optic neuropathy, Endogenous neuroprotection, Cell Survival, Stress-response

Received: 12 Aug 2018; Accepted: 25 Oct 2018.

Edited by:

Andrei Surguchov, University of Kansas Medical Center, United States

Reviewed by:

Kenneth Shindler, University of Pennsylvania, United States
Samuel D. Crish, Northeast Ohio Medical University, United States
Ileana Soto, Rowan University, United States  

Copyright: © 2018 Pietruch-Dutczak, Amadio, Govoni, Lewin-Kowalik and Smedowski. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Dr. Adrian Smedowski, Department of Physiology, Medical University of Silesia, Katowice, Poland, asmedowski@sum.edu.pl