Retinal ischemia: mechanisms of damage and potential therapeutic strategies.
By N. Osborne, R. Casson, J. Wood, G. Chidlow, M. Graham, J. Melena. Progress in retinal and eye research, 2004
1,009 citations recorded by the source corpus.
Subfields: Molecular Biology, Ophthalmology
View Paper: https://www.semanticscholar.org/paper/f90b3526a96d8693a3c2352d4ae80b3d92de24d8
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Citations in the corpus
- Para-inflammation in the aging retina. (2009, background): “In glaucomatous conditions, although mechanical stress is considered a major cause of retinal ganglion cells death, oxidative stress may also play important roles, since it seems to be exaggerated in glaucoma (Fernandez-Durango et al., 2008; Mehdizadeh, 2008; Neufeld, 1999b; Osborne et al., 2004; Za”
- Reperfusion injury and reactive oxygen species: The evolution of a concept (2015, background): “Some examples of these unique functional responses to I/R include arrhythmias and stunning (transient depression of cardiac contractility) for the heart [27,28], behavioral deficits for brain [13], paralysis for spinal cord [18], depressed motility and bacterial translocation (with endotoxemia) for ”
- Oxidative stress in glaucomatous neurodegeneration: mechanisms and consequences. (2006, background): “…in glaucomatous eyes, which is thought to develop secondary to or independent from the elevated IOP, may adversely affect neuronal survival by inducing cell death (Gross et al., 1999; Kitano et al., 1996; Osborne et al., 2004; Rosenbaum et al., 1997; Tezel and Wax, 1999; Tezel and Wax, 2000a).”
- Regulation of retinal blood flow in health and disease. (2008, background): “In the retina, pathophysiological mechanisms of neuronal damage due to ischemia/reperfusion and potential treatment strategies dealing with the prevention or inhibition of neuronal cell loss have been extensively studied (Osborne et al., 2004).”
- Müller cells in the healthy and diseased retina. (2010, background): “The neuronal cell loss accompanying ischemia results mainly from an accumulation of excessive amounts of glutamate, and from an over-stimulation of ionotropic glutamate receptors (Osborne et al., 2004).”