Free Radical Pathways in CNS Injury

By A. Lewén, Paul G. Matz, Pak H. Chan. Journal of Neurotrauma, 2000

821 citations recorded by the source corpus.

Subfields: Biophysics, Molecular Biology, Neurology

View Paper: https://www.semanticscholar.org/paper/1b45bf48cc2dcfbda70ae4ed9ee34aeef24d8c6f

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Citations in the corpus

Acute Spinal Cord Injury, Part I: Pathophysiologic Mechanisms (2001, background): “It has been linked to calcium overload, mitochondrial cytochrome c release, caspase activation, apoptosis, and excitotoxicity (43).”
Ischemia/Reperfusion (2016, neutral): “ment with pharmacological p38 MAPKs inhibitors effectively reduces I/R-induced cell death (324, 431, 491, 494, 571, 637, 763,917).”
Invited Review: Oxidation of Biological Systems: Oxidative Stress Phenomena, Antioxidants, Redox Reactions, and Methods for Their Quantification (2002, background): “radicals, those that produce H2O2, and those responsible for hydroxylation (39, 157, 233).”
Pathophysiology of polytrauma. (2005, background): “Furthermore, oxygen radicals and HOCL activate PMNL to release proteases and collagenase and to inactivate protease-inhibitors (PI).(114) In addition, the capacity of non-enzymatic antioxidants, such as vitamins E or C (scavenger), or enzymatic antioxidants, such as SOD, katalase, or glutathione per”
Secondary injury mechanisms in traumatic spinal cord injury: a nugget of this multiply cascade. (2011, background): “…free radicals (including superoxide, hydroxyl radicals, and nitric oxide and other high-energy oxidants (including peroxynitrite ) are produced during ischemia (Lewen et al. 2000, Bao et al. 2005) with a most pronounced rise during the early reperfusion period (Zini et al. 1992, Nagel et al 2008).”
Cellular Stress Responses, The Hormesis Paradigm, and Vitagenes: Novel Targets for Therapeutic Intervention in Neurodegenerative Disorders (2010, neutral): “Such oxidative damage to membranes is believed to play major roles in a range of disorders, including myocardial infarction (172), stroke and traumatic brain injury (254), and Alzheimer’s disease (AD) (286).”
Inflammation and its role in neuroprotection, axonal regeneration and functional recovery after spinal cord injury. (2008, background): “Free radicals produced during these processes induce apoptosis in neurons and glia via the irreversible oxidation of proteins, lipids and nucleic acids (42;92;95;109;180).”
Neurodegenerative diseases and oxidative stress (2004, background): “cgi?l=7498">xanthine dehydrogenase (also known as xanthine oxidase”
Cell Biology of Ischemia/Reperfusion Injury (2012, background): “It is likely that increased vulnerability of the brain to lipoxidative mediators after IRI contributes to secondary injury (Lewen et al., 2000).”