What can we learn about stroke from retinal ischemia models?
Abstract
Philippe M D’ONOFRIO1, 2, Paulo D KOEBERLE1, *
Faculty of medicine, University of Toronto; 1Division of Anatomy, Department of Surgery, University of Toronto, Canada M5S 1A8; 2Graduate Department of Rehabilitation Science, University of Toronto, Canada M5S 1A8
Retinal ischemia is a very useful model to study the impact of various cell death pathways, such as apoptosis and necrosis, in the ischemic retina. However, it is important to note that the retina is formed as an outpouching of the diencephalon and is part of the central nervous system. As such, the cell death pathways initiated in response to ischemic damage in the retina reflect those found in other areas of the central nervous system undergoing similar trauma. The retina is also more accessible than other areas of the central nervous system, thus making it a simpler model to work with and study. By utilizing the retinal model, we can greatly increase our knowledge of the cell death processes initiated by ischemia which lead to degeneration in the central nervous system. This paper examines work that has been done so far to characterize various aspects of cell death in the retinal ischemia model, such as various pathways which are activated, and the role neurotrophic factors, and discusses how these are relevant to the treatment of ischemic damage in both the retina and the greater central nervous system.
Keywords: ischemia; retina; central nervous system; cell death pathway; apoptosis; necrosis; neurotrophic factor; excitotoxicity
* To whom correspondence should be addressed.
E-mail paulo.koeberle@utoronto.ca
Received 2012-09-19 Accepted 2012-11-06
Keywords:
Faculty of medicine, University of Toronto; 1Division of Anatomy, Department of Surgery, University of Toronto, Canada M5S 1A8; 2Graduate Department of Rehabilitation Science, University of Toronto, Canada M5S 1A8
Retinal ischemia is a very useful model to study the impact of various cell death pathways, such as apoptosis and necrosis, in the ischemic retina. However, it is important to note that the retina is formed as an outpouching of the diencephalon and is part of the central nervous system. As such, the cell death pathways initiated in response to ischemic damage in the retina reflect those found in other areas of the central nervous system undergoing similar trauma. The retina is also more accessible than other areas of the central nervous system, thus making it a simpler model to work with and study. By utilizing the retinal model, we can greatly increase our knowledge of the cell death processes initiated by ischemia which lead to degeneration in the central nervous system. This paper examines work that has been done so far to characterize various aspects of cell death in the retinal ischemia model, such as various pathways which are activated, and the role neurotrophic factors, and discusses how these are relevant to the treatment of ischemic damage in both the retina and the greater central nervous system.
Keywords: ischemia; retina; central nervous system; cell death pathway; apoptosis; necrosis; neurotrophic factor; excitotoxicity
* To whom correspondence should be addressed.
E-mail paulo.koeberle@utoronto.ca
Received 2012-09-19 Accepted 2012-11-06