The Role of Transcription Factors in Regulating the Development and Differentiation of Neural Retina Cells

Document Type : Review Article

Authors

1 Pediatrics Inherited Diseases Research Center, Research Institute for Primordial Prevention of Non-Communicable Disease AND Department of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran

2 Assistant Professor, Pediatrics Inherited Diseases Research Center, Research Institute for Primordial Prevention of Non-Communicable Disease AND Department of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran

Abstract

Neural retina is the part of the diencephalon and because of the relatively simple structure in known as a suitable model for studying the molecular mechanisms of the central nervous system. Visual perception is the result of the function of six types of neurons organized in the structure of the neural retina. Neural retina develops via the proliferation of a common precursor cell in the inner layer of the optic cup. Retinal progenitor cell acquires the competent to differentiate into different cell fates by different factors in a time-dependent and protected manner in the mammals. Destruction and loss of these cells in the retina occurs in various retinal diseases and impairs the process of human vision. Lack of reconstruction of damaged nerve cells in the retina of mammals, including humans is a noted problem; and in recent decades, a wide range of research in the eye field allocated the possibility of replacing the retinal cells and many efforts is made to treat these diseases. Study and identifying the transcription factors involved in neuronal differentiation can provide a useful tool for gene therapy aiming to regenerate retinal neurons in the near future.

Keywords

References

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Journal of Isfahan Medical School
Volume 33, Issue 351 - Serial Number 351
July and August 2015
Pages 1584-1596

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History

  • Receive Date: 26 November 2014
  • Revise Date: 01 November 2024
  • Accept Date: 06 April 2022

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