What can we learn about stroke from retinal ischemia models?

被引:38
作者
D'Onofrio, Philippe M. [1 ,2 ]
Koeberle, Paulo D. [1 ]
机构
[1] Univ Toronto, Dept Surg, Div Anat, Toronto, ON M5S 1A8, Canada
[2] Univ Toronto, Grad Dept Rehabil Sci, Toronto, ON M5S 1A8, Canada
关键词
ischemia; retina; central nervous system; cell death pathway; apoptosis; necrosis; neurotrophic factor; excitotoxicity; NERVE GROWTH-FACTOR; CILIARY NEUROTROPHIC FACTOR; CELLS IN-VIVO; GLUTAMATE-INDUCED EXCITOTOXICITY; AMYOTROPHIC-LATERAL-SCLEROSIS; OXYGEN-GLUCOSE DEPRIVATION; FOCAL CEREBRAL-ISCHEMIA; ADULT-RAT RETINA; GANGLION-CELLS; OPTIC-NERVE;
D O I
10.1038/aps.2012.165
中图分类号
O6 [化学];
学科分类号
070301 [无机化学];
摘要
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.
引用
收藏
页码:91 / 103
页数:13
相关论文
共 218 条
[1]
Ocular neuroprotection by siRNA targeting caspase-2 [J].
Ahmed, Z. ;
Kalinski, H. ;
Berry, M. ;
Almasieh, M. ;
Ashush, H. ;
Slager, N. ;
Brafman, A. ;
Spivak, I. ;
Prasad, N. ;
Mett, I. ;
Shalom, E. ;
Alpert, E. ;
Di Polo, A. ;
Feinstein, E. ;
Logan, A. .
CELL DEATH & DISEASE, 2011, 2 :e173-e173
[2]
Death receptors: Signaling and modulation [J].
Ashkenazi, A ;
Dixit, VM .
SCIENCE, 1998, 281 (5381) :1305-1308
[3]
ACh receptors link two signaling pathways to neuroprotection against glutamate-induced excitotoxicity in isolated RGCs [J].
Asomugha, Chinwe O. ;
Linn, David M. ;
Linn, Cindy L. .
JOURNAL OF NEUROCHEMISTRY, 2010, 112 (01) :214-226
[4]
FUNCTIONAL STATUS INFLUENCES THE ABILITY OF SCHWANN-CELLS TO SUPPORT ADULT-RAT RETINAL GANGLION-CELL SURVIVAL AND AXONAL REGROWTH [J].
BAEHR, M ;
BUNGE, RP .
EXPERIMENTAL NEUROLOGY, 1989, 106 (01) :27-40
[5]
Retinal signs and stroke - Revisiting the link between the eye and brain [J].
Baker, Michelle L. ;
Hand, Peter J. ;
Wang, Jie Jin ;
Wong, Tien Y. .
STROKE, 2008, 39 (04) :1371-1379
[6]
The GDNF family ligands and receptors - implications for neural development [J].
Baloh, RH ;
Enomoto, H ;
Johnson, EM ;
Milbrandt, J .
CURRENT OPINION IN NEUROBIOLOGY, 2000, 10 (01) :103-110
[7]
The crystal structure of caspase-6, a selective effector of axonal degeneration [J].
Baumgartner, Renato ;
Meder, Gabriele ;
Briand, Christophe ;
Decock, Arnaud ;
D'Arcy, Allan ;
Hassiepen, Ulrich ;
Morse, Richard ;
Renatus, Martin .
BIOCHEMICAL JOURNAL, 2009, 423 :429-439
[8]
NEUROTROPHIN-5 - A NOVEL NEUROTROPHIC FACTOR THAT ACTIVATES TRK AND TRKB [J].
BERKEMEIER, LR ;
WINSLOW, JW ;
KAPLAN, DR ;
NIKOLICS, K ;
GOEDDEL, DV ;
ROSENTHAL, A .
NEURON, 1991, 7 (05) :857-866
[9]
New hope for stroke patients: mobilization of endogenous stem cells [J].
Borlongan, CV ;
Hess, DC .
CANADIAN MEDICAL ASSOCIATION JOURNAL, 2006, 174 (07) :954-955
[10]
Cell shrinkage and monovalent cation fluxes: Role in apoptosis [J].
Bortner, Carl D. ;
Cidlowski, John A. .
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, 2007, 462 (02) :176-188