Open Access
REVIEW
Contribution of TNF-α to the development of retinal neurodegenerative disorders
1 Department of Biochemistry, Faculty of Pharmacy, University of Mansoura, Egypt
2 Department of Pharmacology and Biochemistry, Faculty of Pharmacy, Delta University for Science and Technology, Egypt
* Corresponding Author: MMH Al-Gayyar,
European Cytokine Network 2013, 24(1), 27-36. https://doi.org/10.1684/ecn.2013.0334
Abstract
During the late 1970s, tumor necrosis factor alpha (TNF-α) was initially recognized as an endotoxin-induced substance that was mainly produced by macrophages, and able to cause the lysis of certain tumor cells. Subsequent research demonstrated that TNF-α mediates a broad range of cellular activities, including proliferation, survival, differentiation and apoptosis. It is also considered to be essential for the induction and maintenance of the inflammatory immune responses. Meanwhile, visual impairment imposes a substantial disease burden on society. It is associated with both significant economic impact and reduction in quality of life. Visual impairment raises serious social challenges for both patients and their families, interfering with day-to-day life, and can limit employment possibilities.Many of the most common, irreversible blinding pathologies involve neuronal loss from the retina, which is the light-sensing tissue of the eye. The retina, being part of the central nervous system, is unable to regenerate neurons lost to disease. Therefore, in the current review we will discuss the association between increased expression of TNF-α with neurodegenerative disorders, downstream cellular signaling mechanisms following interaction of TNF-α with its receptors, and the role of TNF-α as a possible target in the treatment of retinal neurodegenerative disorders.Keywords
Cite This Article
Copyright © 2013 The Author(s). Published by Tech Science Press.This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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