Oxidative stress and nitration in neurodegeneration: cause, effect, or association?
By H. Ischiropoulos, J. Beckman. Journal of Clinical Investigation, 2003
706 citations recorded by the source corpus.
Subfields: Neurology
View Paper: https://www.semanticscholar.org/paper/4c706fcd596dcc47facc0c3cb2c2f6a39608168b
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In Neurology
- Valina L. Dawson
- T. Dawson
- M. Mouradian
- Christoph Handschin
- V. Dias
- E. Junn
- B. Spiegelman
- Mark P. Mattson
Citations in the corpus
- Molecular pathophysiology of Parkinson's disease. (2005, background): “…paraquat clearly lead to aggregation and accumulation of α-synuclein in vitro and in animal models (Betarbet et al. 2000; Manning- Bog et al. 2002; Sherer et al. 2002b, 2003), and other forms of oxidative and nitrosative stress also promote α-synuclein aggregation (Ischiropoulos & Beckman 2003).”
- Metabolic control through the PGC-1 family of transcription coactivators. (2005, background): “It is now clear that ROS generation is greatly elevated following certain metabolic perturbation, such as ischemia reperfusion of the heart, stroke in the brain, as well as a wide range of disorders including neurodegenerative diseases (Ischiropoulos and Beckman, 2003).”
- S-nitrosylated GAPDH initiates apoptotic cell death by nuclear translocation following Siah1 binding (2005, background): “Cell stress causes the formation of several reactive oxygen specie”
- The Role of Oxidative Stress in Parkinson’s Disease (2013, background): “Fibrils of alpha-synuclein are present in Lewy bodies [225], and the formation of aggregates is associated with increased oxidative or nitrosative stress [107, 226, 227].”
- Iron metabolism and toxicity. (2005, background): “An increase in the steady state levels of reactive oxygen (and nitrogen) species beyond the antioxidant capacity of the organism, called oxidative (and nitrosative) stress, is encountered in many pathological conditions, such as chronic inflammation, ischemia–reperfusion injury, or neurodegeneration”